14th INTERNATIONAL SYMPOSIUM ON 14th INTERNATIONAL SYMPOSIUM ON 14th INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION (ISNR) NEURAL REGENERATION (ISNR) NEURAL REGENERATION (ISNR) Dr. Roger Madison, Director Dr. Roger Madison, Director Dr. Roger Madison, Director

December 7th-11th, 2011 December 7th-11th, 2011 December 7th-11th, 2011 Asilomar Conference Center Asilomar Conference Center Asilomar Conference Center Pacific Grove, CA Pacific Grove, CA Pacific Grove, CA USA USA USA

Hosted by: Hosted by: Hosted by: International Symposium on Neural Regeneration International Symposium on Neural Regeneration International Symposium on Neural Regeneration U.S. Department of Veterans Affairs U.S. Department of Veterans Affairs U.S. Department of Veterans Affairs (Biomedical Laboratory Research and Development Service) (Biomedical Laboratory Research and Development Service) (Biomedical Laboratory Research and Development Service) (Office of Research and Development) (Office of Research and Development) (Office of Research and Development)

Cosponsored by: Cosponsored by: Cosponsored by: National Institutes of Health (National Institute of Neurological Disorders and Stroke) National Institutes of Health (National Institute of Neurological Disorders and Stroke) National Institutes of Health (National Institute of Neurological Disorders and Stroke) California Institute for Regenerative Medicine (CIRM) California Institute for Regenerative Medicine (CIRM) California Institute for Regenerative Medicine (CIRM) Paralyzed Veterans of America (Education Foundation) Paralyzed Veterans of America (Education Foundation) Paralyzed Veterans of America (Education Foundation) International Society for Neurochemistry (ISN) International Society for Neurochemistry (ISN) International Society for Neurochemistry (ISN) Mission Connect – A Project of TIRR Foundation Mission Connect – A Project of TIRR Foundation Mission Connect – A Project of TIRR Foundation

Information about the symposia series can be obtained from the conference Web site Information about the symposia series can be obtained from the conference Web site Information about the symposia series can be obtained from the conference Web site (www.rehab.research.va.gov/ISNR), from the directors office via email: [email protected], (www.rehab.research.va.gov/ISNR), from the directors office via email: [email protected], (www.rehab.research.va.gov/ISNR), from the directors office via email: [email protected], or by calling (919) 286-0411 x7691. or by calling (919) 286-0411 x7691. or by calling (919) 286-0411 x7691.

1 1 1 2 2 2 THE FOURTEENTH INTERNATIONAL THE FOURTEENTH INTERNATIONAL THE FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION SYMPOSIUM ON NEURAL REGENERATION SYMPOSIUM ON NEURAL REGENERATION

December 7-11, 2011 December 7-11, 2011 December 7-11, 2011

Asilomar Conference Grounds Phone: (813) 642-4222 Asilomar Conference Grounds Phone: (813) 642-4222 Asilomar Conference Grounds Phone: (813) 642-4222 800 Asilomar Boulevard Fax: (813) 642-4261 800 Asilomar Boulevard Fax: (813) 642-4261 800 Asilomar Boulevard Fax: (813) 642-4261 Pacific Grove, California 93950 Web: www.visitasilomar.com Pacific Grove, California 93950 Web: www.visitasilomar.com Pacific Grove, California 93950 Web: www.visitasilomar.com

SYMPOSIUM DIRECTOR SYMPOSIUM DIRECTOR SYMPOSIUM DIRECTOR Roger D. Madison (VA Medical Center and Duke University – Durham, NC) Roger D. Madison (VA Medical Center and Duke University – Durham, NC) Roger D. Madison (VA Medical Center and Duke University – Durham, NC)

PROGRAM PLANNING COMMITTEE PROGRAM PLANNING COMMITTEE PROGRAM PLANNING COMMITTEE Jacqueline Bresnahan (University of California, San Francisco, CA) Jacqueline Bresnahan (University of California, San Francisco, CA) Jacqueline Bresnahan (University of California, San Francisco, CA) David Gardiner (University of California, Irvine, CA) David Gardiner (University of California, Irvine, CA) David Gardiner (University of California, Irvine, CA) James Guest (University of Miami – Miami, FL) James Guest (University of Miami – Miami, FL) James Guest (University of Miami – Miami, FL) Jane Lebkowski (Geron Corporation, Menlo Park, CA) Jane Lebkowski (Geron Corporation, Menlo Park, CA) Jane Lebkowski (Geron Corporation, Menlo Park, CA) David Shine (Baylor College of Medicine/Houston VA Medical Center – Houston, TX) David Shine (Baylor College of Medicine/Houston VA Medical Center – Houston, TX) David Shine (Baylor College of Medicine/Houston VA Medical Center – Houston, TX) John Steeves (ICORD/University of British Columbia – Vancouver, BC, Canada) John Steeves (ICORD/University of British Columbia – Vancouver, BC, Canada) John Steeves (ICORD/University of British Columbia – Vancouver, BC, Canada)

Guest Participants: Guest Participants: Guest Participants: Audrey Kusiak (VA Rehabilitation Research and Development – Washington, DC) Audrey Kusiak (VA Rehabilitation Research and Development – Washington, DC) Audrey Kusiak (VA Rehabilitation Research and Development – Washington, DC) Naomi Kleitman (NIH/National Institute of Neurological Disorders and Stroke – Bethesda, MD) Naomi Kleitman (NIH/National Institute of Neurological Disorders and Stroke – Bethesda, MD) Naomi Kleitman (NIH/National Institute of Neurological Disorders and Stroke – Bethesda, MD)

PROGRAM AND TECHNICAL ASSISTANTS PROGRAM AND TECHNICAL ASSISTANTS PROGRAM AND TECHNICAL ASSISTANTS Frances Stuart (VA Medical Center – Durham, NC) Frances Stuart (VA Medical Center – Durham, NC) Frances Stuart (VA Medical Center – Durham, NC) Qiang Li (VA Medical Center and Duke University – Durham, NC) Qiang Li (VA Medical Center and Duke University – Durham, NC) Qiang Li (VA Medical Center and Duke University – Durham, NC) Chris McGee (VA Medical Center – Durham, NC) Chris McGee (VA Medical Center – Durham, NC) Chris McGee (VA Medical Center – Durham, NC) Rod Williams (International Symposium on Neural Regeneration) Rod Williams (International Symposium on Neural Regeneration) Rod Williams (International Symposium on Neural Regeneration)

ACKNOWLEDGEMENTS ACKNOWLEDGEMENTS ACKNOWLEDGEMENTS The symposium is sponsored by the US Department of Veterans Affairs (Biomedical Laboratory Research The symposium is sponsored by the US Department of Veterans Affairs (Biomedical Laboratory Research The symposium is sponsored by the US Department of Veterans Affairs (Biomedical Laboratory Research and Development Service, Office of Research and Development), the Paralyzed Veterans of America and Development Service, Office of Research and Development), the Paralyzed Veterans of America and Development Service, Office of Research and Development), the Paralyzed Veterans of America (Education Foundation), the National Institutes of Health (National Institute of Neurological Disorders (Education Foundation), the National Institutes of Health (National Institute of Neurological Disorders (Education Foundation), the National Institutes of Health (National Institute of Neurological Disorders and Stroke), California Institute for Regenerative Medicine, International Society for Neurochemistry and and Stroke), California Institute for Regenerative Medicine, International Society for Neurochemistry and and Stroke), California Institute for Regenerative Medicine, International Society for Neurochemistry and Mission Connect (A Project of TIRR Foundation). Mission Connect (A Project of TIRR Foundation). Mission Connect (A Project of TIRR Foundation).

3 3 3 INTRODUCTION INTRODUCTION INTRODUCTION

The Fourteenth International Symposium on Neural Regeneration will be held at the Asilomar Conference The Fourteenth International Symposium on Neural Regeneration will be held at the Asilomar Conference The Fourteenth International Symposium on Neural Regeneration will be held at the Asilomar Conference Center in Pacific Grove, California from December 7-11, 2011. The International Symposium on Neural Center in Pacific Grove, California from December 7-11, 2011. The International Symposium on Neural Center in Pacific Grove, California from December 7-11, 2011. The International Symposium on Neural Regeneration began in 1985, and has been held on a biennial basis since that time. The primary sponsor Regeneration began in 1985, and has been held on a biennial basis since that time. The primary sponsor Regeneration began in 1985, and has been held on a biennial basis since that time. The primary sponsor has been the Department of Veterans Affairs, with the NIH continuously co-sponsoring the symposia has been the Department of Veterans Affairs, with the NIH continuously co-sponsoring the symposia has been the Department of Veterans Affairs, with the NIH continuously co-sponsoring the symposia since 1987. Long term generous support has also been given by the Paralyzed Veterans of America. since 1987. Long term generous support has also been given by the Paralyzed Veterans of America. since 1987. Long term generous support has also been given by the Paralyzed Veterans of America. Current ISNR funding has also been received from the California Institute for Regenerative Medicine, the Current ISNR funding has also been received from the California Institute for Regenerative Medicine, the Current ISNR funding has also been received from the California Institute for Regenerative Medicine, the International Society for Neurochemistry and Mission Connect, which is a project of TIRR Foundation. International Society for Neurochemistry and Mission Connect, which is a project of TIRR Foundation. International Society for Neurochemistry and Mission Connect, which is a project of TIRR Foundation. The generous support of all of our sponsors is gratefully acknowledged. The generous support of all of our sponsors is gratefully acknowledged. The generous support of all of our sponsors is gratefully acknowledged.

The keynote speakers for this year’s symposium will be Mark Tuszynski from the University of The keynote speakers for this year’s symposium will be Mark Tuszynski from the University of The keynote speakers for this year’s symposium will be Mark Tuszynski from the University of California, San Diego and the San Diego VA Medical Center. Featured talks will be given by Hunter California, San Diego and the San Diego VA Medical Center. Featured talks will be given by Hunter California, San Diego and the San Diego VA Medical Center. Featured talks will be given by Hunter Peckham from Case Western Reserve University and the Cleveland VA Medical Center; Colin McCaig Peckham from Case Western Reserve University and the Cleveland VA Medical Center; Colin McCaig Peckham from Case Western Reserve University and the Cleveland VA Medical Center; Colin McCaig from the University of Aberdeen; Dwight Bergles from the Johns Hopkins School of Medicine; Stefan from the University of Aberdeen; Dwight Bergles from the Johns Hopkins School of Medicine; Stefan from the University of Aberdeen; Dwight Bergles from the Johns Hopkins School of Medicine; Stefan Heller from Stanford University School of Medicine and Ed Boyden from Massachusetts Institute of Heller from Stanford University School of Medicine and Ed Boyden from Massachusetts Institute of Heller from Stanford University School of Medicine and Ed Boyden from Massachusetts Institute of Technology. Following the format of preceding neural regeneration symposia, the program is divided into Technology. Following the format of preceding neural regeneration symposia, the program is divided into Technology. Following the format of preceding neural regeneration symposia, the program is divided into six sessions, including: 1) Brain Machine Interface, chaired by Doug Weber; 2) DEBATE – The future of six sessions, including: 1) Brain Machine Interface, chaired by Doug Weber; 2) DEBATE – The future of six sessions, including: 1) Brain Machine Interface, chaired by Doug Weber; 2) DEBATE – The future of functional recovery is robotics not regeneration, moderated by Dave Shine; 3) Stem Cells – The promises functional recovery is robotics not regeneration, moderated by Dave Shine; 3) Stem Cells – The promises functional recovery is robotics not regeneration, moderated by Dave Shine; 3) Stem Cells – The promises and challenges, chaired by Itzhak Fischer; 4) Translational Approaches, chaired by Naomi Kleitman; 5) and challenges, chaired by Itzhak Fischer; 4) Translational Approaches, chaired by Naomi Kleitman; 5) and challenges, chaired by Itzhak Fischer; 4) Translational Approaches, chaired by Naomi Kleitman; 5) ISN Symposium on Neurochemistry and Neurobiology of Repair, chaired by Jacqueline Bresnahan; and ISN Symposium on Neurochemistry and Neurobiology of Repair, chaired by Jacqueline Bresnahan; and ISN Symposium on Neurochemistry and Neurobiology of Repair, chaired by Jacqueline Bresnahan; and 6) Route 28 Summit Presentations – Novel ways to exploit stem cells for recovery of CNS function, 6) Route 28 Summit Presentations – Novel ways to exploit stem cells for recovery of CNS function, 6) Route 28 Summit Presentations – Novel ways to exploit stem cells for recovery of CNS function, chaired by Theo Palmer. The abstracts for the speaker presentations as well as 87 poster presentations are chaired by Theo Palmer. The abstracts for the speaker presentations as well as 87 poster presentations are chaired by Theo Palmer. The abstracts for the speaker presentations as well as 87 poster presentations are given in the program on the following pages. given in the program on the following pages. given in the program on the following pages.

The primary purpose of the symposium is to present current work in neural regeneration, especially in The primary purpose of the symposium is to present current work in neural regeneration, especially in The primary purpose of the symposium is to present current work in neural regeneration, especially in those areas of research in which there has been some notable recent progress or in which some those areas of research in which there has been some notable recent progress or in which some those areas of research in which there has been some notable recent progress or in which some particularly interesting issues have been raised. A secondary purpose is to foster an atmosphere that is particularly interesting issues have been raised. A secondary purpose is to foster an atmosphere that is particularly interesting issues have been raised. A secondary purpose is to foster an atmosphere that is both stimulating and conducive to a free interchange of ideas among investigators, or between seasoned both stimulating and conducive to a free interchange of ideas among investigators, or between seasoned both stimulating and conducive to a free interchange of ideas among investigators, or between seasoned investigators and students. The International Neural Regeneration Symposium has become an established, investigators and students. The International Neural Regeneration Symposium has become an established, investigators and students. The International Neural Regeneration Symposium has become an established, regularly occurring event with high attendance by both students as well as internationally recognized regularly occurring event with high attendance by both students as well as internationally recognized regularly occurring event with high attendance by both students as well as internationally recognized experts in the field of neural regeneration. experts in the field of neural regeneration. experts in the field of neural regeneration.

Roger Madison,, Ph.D. Roger Madison,, Ph.D. Roger Madison,, Ph.D. Director, International Symposium on Neural Regeneration Director, International Symposium on Neural Regeneration Director, International Symposium on Neural Regeneration Laboratory of Nerve Regeneration Laboratory of Nerve Regeneration Laboratory of Nerve Regeneration Duke University Medical Center Duke University Medical Center Duke University Medical Center Research Career Scientist Research Career Scientist Research Career Scientist Veterans Affairs Medical Center Veterans Affairs Medical Center Veterans Affairs Medical Center Building/16/Room 38 Building/16/Room 38 Building/16/Room 38 508 Fulton Street 508 Fulton Street 508 Fulton Street Durham, NC 27705 Durham, NC 27705 Durham, NC 27705

4 4 4 TABLE OF CONTENTS TABLE OF CONTENTS TABLE OF CONTENTS

Host and Sponsors…………………………………………………………………… 1 Host and Sponsors…………………………………………………………………… 1 Host and Sponsors…………………………………………………………………… 1

Committee and Acknowledgements………………………………………………… 3 Committee and Acknowledgements………………………………………………… 3 Committee and Acknowledgements………………………………………………… 3

Introduction: Fourteenth International Symposium on Neural Regeneration………. 4 Introduction: Fourteenth International Symposium on Neural Regeneration………. 4 Introduction: Fourteenth International Symposium on Neural Regeneration………. 4

Scientific Program……………………………………………………………….….. 7 Scientific Program……………………………………………………………….….. 7 Scientific Program……………………………………………………………….….. 7

Oral Presentations……………………………………………………………………13 Oral Presentations……………………………………………………………………13 Oral Presentations……………………………………………………………………13

Overview - Poster Presentations………………………………………………….….25 Overview - Poster Presentations………………………………………………….….25 Overview - Poster Presentations………………………………………………….….25

Abstracts of Poster Presentations – Session One………………………………….…34 Abstracts of Poster Presentations – Session One………………………………….…34 Abstracts of Poster Presentations – Session One………………………………….…34

Abstracts of Poster Presentations – Session Two……………………………….…...64 Abstracts of Poster Presentations – Session Two……………………………….…...64 Abstracts of Poster Presentations – Session Two……………………………….…...64

Author Index……………………………………………………………………..…..90 Author Index……………………………………………………………………..…..90 Author Index……………………………………………………………………..…..90

5 5 5 6 6 6 14th International Symposium on Neural Regeneration 14th International Symposium on Neural Regeneration 14th International Symposium on Neural Regeneration Scientific Program Scientific Program Scientific Program

WEDNESDAY – DECEMBER 7, 2011 WEDNESDAY – DECEMBER 7, 2011 WEDNESDAY – DECEMBER 7, 2011

3:00 PM Arrival of participants and check-in 3:00 PM Arrival of participants and check-in 3:00 PM Arrival of participants and check-in

6:00 PM DINNER 6:00 PM DINNER 6:00 PM DINNER

7:30 PM Welcome and Keynote Address 7:30 PM Welcome and Keynote Address 7:30 PM Welcome and Keynote Address

Keynote Speaker: Mark Tuszynski Keynote Speaker: Mark Tuszynski Keynote Speaker: Mark Tuszynski University of California, San Diego University of California, San Diego University of California, San Diego San Diego VAMC San Diego VAMC San Diego VAMC San Diego, CA - USA San Diego, CA - USA San Diego, CA - USA “Combinatorial Strategies for Regeneration After Spinal Cord Injury” “Combinatorial Strategies for Regeneration After Spinal Cord Injury” “Combinatorial Strategies for Regeneration After Spinal Cord Injury”

THURSDAY – DECEMBER 8, 2011 THURSDAY – DECEMBER 8, 2011 THURSDAY – DECEMBER 8, 2011

Session One: 8:15 am Session One: 8:15 am Session One: 8:15 am Brain Machine Interface (BMI) Brain Machine Interface (BMI) Brain Machine Interface (BMI)

8:15 AM Chair: Doug Weber 8:15 AM Chair: Doug Weber 8:15 AM Chair: Doug Weber University of Pittsburgh University of Pittsburgh University of Pittsburgh Pittsburgh VAMC Pittsburgh VAMC Pittsburgh VAMC Pittsburgh, PA - USA Pittsburgh, PA - USA Pittsburgh, PA - USA

8:30 AM Andrea Kubler 8:30 AM Andrea Kubler 8:30 AM Andrea Kubler University of Wurzburg University of Wurzburg University of Wurzburg Germany Germany Germany “Out of the frying pan into the fire – BCI faces real world application” “Out of the frying pan into the fire – BCI faces real world application” “Out of the frying pan into the fire – BCI faces real world application”

9:00 AM Bradley Greger 9:00 AM Bradley Greger 9:00 AM Bradley Greger University of Utah University of Utah University of Utah Salt Lake City, UT - USA Salt Lake City, UT - USA Salt Lake City, UT - USA “Micro-electrodes in and on the cerebral cortex for decoding and encoding “Micro-electrodes in and on the cerebral cortex for decoding and encoding “Micro-electrodes in and on the cerebral cortex for decoding and encoding information” information” information”

9:30 AM Chet Moritz 9:30 AM Chet Moritz 9:30 AM Chet Moritz University of Washington University of Washington University of Washington Seattle, WA - USA Seattle, WA - USA Seattle, WA - USA “Leveraging neural plasticity for the treatment of paralysis and other movement “Leveraging neural plasticity for the treatment of paralysis and other movement “Leveraging neural plasticity for the treatment of paralysis and other movement disorders” disorders” disorders”

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 7 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 7 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 7

10:00 AM Jennifer Collinger 10:00 AM Jennifer Collinger 10:00 AM Jennifer Collinger University of Pittsburgh University of Pittsburgh University of Pittsburgh Pittsburgh VAMC Pittsburgh VAMC Pittsburgh VAMC Pittsburgh, PA - USA Pittsburgh, PA - USA Pittsburgh, PA - USA “Is BCI technology ready for prime time? The science is mature and the “Is BCI technology ready for prime time? The science is mature and the “Is BCI technology ready for prime time? The science is mature and the consumers are willing - what are we waiting for?” consumers are willing - what are we waiting for?” consumers are willing - what are we waiting for?”

11:00 AM Featured Speaker 11:00 AM Featured Speaker 11:00 AM Featured Speaker Hunter Peckham Hunter Peckham Hunter Peckham Case Western Reserve University Case Western Reserve University Case Western Reserve University Cleveland VAMC Cleveland VAMC Cleveland VAMC Cleveland, OH - USA Cleveland, OH - USA Cleveland, OH - USA “The Role of Neural Prosthesis and Neural Stimulation In the Restoration of “The Role of Neural Prosthesis and Neural Stimulation In the Restoration of “The Role of Neural Prosthesis and Neural Stimulation In the Restoration of Function” Function” Function”

12:00 Noon LUNCH 12:00 Noon LUNCH 12:00 Noon LUNCH

1:00 PM Featured Speaker 1:00 PM Featured Speaker 1:00 PM Featured Speaker Colin McCaig Colin McCaig Colin McCaig University of Aberdeen University of Aberdeen University of Aberdeen Scotland Scotland Scotland “Regulating neural cell behaviour with extracellular electrical signals” “Regulating neural cell behaviour with extracellular electrical signals” “Regulating neural cell behaviour with extracellular electrical signals”

2:00 PM Viewing: Poster Session 1 2:00 PM Viewing: Poster Session 1 2:00 PM Viewing: Poster Session 1

6:00 PM DINNER 6:00 PM DINNER 6:00 PM DINNER

Session Two: 7:15 PM – 9:00 PM (or beyond) Session Two: 7:15 PM – 9:00 PM (or beyond) Session Two: 7:15 PM – 9:00 PM (or beyond) DEBATE – Proposition: The future of functional recovery is robotics not regeneration DEBATE – Proposition: The future of functional recovery is robotics not regeneration DEBATE – Proposition: The future of functional recovery is robotics not regeneration

7:15 PM Moderator: Dave Shine 7:15 PM Moderator: Dave Shine 7:15 PM Moderator: Dave Shine Baylor College of Medicine Baylor College of Medicine Baylor College of Medicine Houston VAMC Houston VAMC Houston VAMC Houston, TX - USA Houston, TX - USA Houston, TX - USA

Affirmative: Vivian Mushahwar Affirmative: Vivian Mushahwar Affirmative: Vivian Mushahwar University of Alberta University of Alberta University of Alberta Edmonton, Alberta, Canada Edmonton, Alberta, Canada Edmonton, Alberta, Canada

Chet Moritz Chet Moritz Chet Moritz University of Washington University of Washington University of Washington Seattle, WA - USA Seattle, WA - USA Seattle, WA - USA

Doug Weber Doug Weber Doug Weber University of Pittsburgh University of Pittsburgh University of Pittsburgh

8 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 8 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 8 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION Pittsburgh VAMC Pittsburgh VAMC Pittsburgh VAMC Pittsburgh, PA - USA Pittsburgh, PA - USA Pittsburgh, PA - USA

Alan Harvey Alan Harvey Alan Harvey University of Western Australia University of Western Australia University of Western Australia Crawley, Western Australia Crawley, Western Australia Crawley, Western Australia

Negative: Hunter Peckham Negative: Hunter Peckham Negative: Hunter Peckham Case Western Reserve University Case Western Reserve University Case Western Reserve University Cleveland VAMC Cleveland VAMC Cleveland VAMC Cleveland, OH - USA Cleveland, OH - USA Cleveland, OH - USA

Linda Noble-Hauesslein Linda Noble-Hauesslein Linda Noble-Hauesslein University of California, San Francisco University of California, San Francisco University of California, San Francisco San Francisco, CA - USA San Francisco, CA - USA San Francisco, CA - USA

Jerry Silver Jerry Silver Jerry Silver Case Western Reserve University Case Western Reserve University Case Western Reserve University Cleveland, OH - USA Cleveland, OH - USA Cleveland, OH - USA

Arthur Prochazka Arthur Prochazka Arthur Prochazka University of Alberta University of Alberta University of Alberta Edmonton, Alberta, Canada Edmonton, Alberta, Canada Edmonton, Alberta, Canada

FRIDAY – DECEMBER 9, 2011 FRIDAY – DECEMBER 9, 2011 FRIDAY – DECEMBER 9, 2011

Session Three: 8:15 AM Session Three: 8:15 AM Session Three: 8:15 AM Stem Cells – The promises and challenges Stem Cells – The promises and challenges Stem Cells – The promises and challenges

8:15 AM Chair: Itzhak Fischer 8:15 AM Chair: Itzhak Fischer 8:15 AM Chair: Itzhak Fischer Drexel University Drexel University Drexel University Philadelphia, PA - USA Philadelphia, PA - USA Philadelphia, PA - USA

8:30 AM Mathew Blurton-Jones 8:30 AM Mathew Blurton-Jones 8:30 AM Mathew Blurton-Jones University of California, Irvine University of California, Irvine University of California, Irvine Irvine, CA - USA Irvine, CA - USA Irvine, CA - USA “Can Neural Stem Cells be used to treat Alzheimer disease?” “Can Neural Stem Cells be used to treat Alzheimer disease?” “Can Neural Stem Cells be used to treat Alzheimer disease?”

9:00 AM Itzhak Fischer 9:00 AM Itzhak Fischer 9:00 AM Itzhak Fischer Drexel University Drexel University Drexel University Philadelphia, PA - USA Philadelphia, PA - USA Philadelphia, PA - USA “Transplanting neural stem cells to reconnect the injured spinal cord” “Transplanting neural stem cells to reconnect the injured spinal cord” “Transplanting neural stem cells to reconnect the injured spinal cord”

9:30 AM Nicholas Maragakis 9:30 AM Nicholas Maragakis 9:30 AM Nicholas Maragakis Johns Hopkins School of Medicine Johns Hopkins School of Medicine Johns Hopkins School of Medicine Baltimore, MD - USA Baltimore, MD - USA Baltimore, MD - USA

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 9 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 9 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 9 “Scientific and Clinical Challenges in using Stem Cells for Investigating and “Scientific and Clinical Challenges in using Stem Cells for Investigating and “Scientific and Clinical Challenges in using Stem Cells for Investigating and Treating Amyotrophic Lateral Sclerosis” Treating Amyotrophic Lateral Sclerosis” Treating Amyotrophic Lateral Sclerosis”

10:00 AM Gary Steinberg 10:00 AM Gary Steinberg 10:00 AM Gary Steinberg Stanford University School of Medicine Stanford University School of Medicine Stanford University School of Medicine Stanford, CA - USA Stanford, CA - USA Stanford, CA - USA “Neural Stem Cell Therapy for Stroke: Underlying Mechanisms and Clinical “Neural Stem Cell Therapy for Stroke: Underlying Mechanisms and Clinical “Neural Stem Cell Therapy for Stroke: Underlying Mechanisms and Clinical Translation” Translation” Translation”

10:30 AM BREAK 10:30 AM BREAK 10:30 AM BREAK

11:00 AM Featured Speaker 11:00 AM Featured Speaker 11:00 AM Featured Speaker Dwight Bergles Dwight Bergles Dwight Bergles Johns Hopkins School of Medicine Johns Hopkins School of Medicine Johns Hopkins School of Medicine Baltimore, MD - USA Baltimore, MD - USA Baltimore, MD - USA “Fate and function of glial progenitors in the mammalian CNS” “Fate and function of glial progenitors in the mammalian CNS” “Fate and function of glial progenitors in the mammalian CNS”

12:00 Noon LUNCH 12:00 Noon LUNCH 12:00 Noon LUNCH

1:00 PM Featured Speaker 1:00 PM Featured Speaker 1:00 PM Featured Speaker Stefan Heller Stefan Heller Stefan Heller Stanford University School of Medicine Stanford University School of Medicine Stanford University School of Medicine Stanford, CA - USA Stanford, CA - USA Stanford, CA - USA “Inner ear sensory hair cells from stem cells” “Inner ear sensory hair cells from stem cells” “Inner ear sensory hair cells from stem cells”

Session Four: 7:15 - 9:00 PM Session Four: 7:15 - 9:00 PM Session Four: 7:15 - 9:00 PM Translational Approaches – “Lost in Translation” Translational Approaches – “Lost in Translation” Translational Approaches – “Lost in Translation”

7:15 PM Chair: Naomi Kleitman 7:15 PM Chair: Naomi Kleitman 7:15 PM Chair: Naomi Kleitman NIH/NINDS NIH/NINDS NIH/NINDS Bethesda, MD - USA Bethesda, MD - USA Bethesda, MD - USA “Implications Of Replications: Improving The Quality Of Preclinical Research” “Implications Of Replications: Improving The Quality Of Preclinical Research” “Implications Of Replications: Improving The Quality Of Preclinical Research”

7:45 PM David Howells 7:45 PM David Howells 7:45 PM David Howells University of Melbourne University of Melbourne University of Melbourne Melbourne, Australia Melbourne, Australia Melbourne, Australia “Avoiding bias at the bench” “Avoiding bias at the bench” “Avoiding bias at the bench”

8:15 PM Dan Lammertse 8:15 PM Dan Lammertse 8:15 PM Dan Lammertse Craig Hospital Craig Hospital Craig Hospital University of Colorado, Denver University of Colorado, Denver University of Colorado, Denver Denver, CO - USA Denver, CO - USA Denver, CO - USA “The Challenges of Translation: A Clinical Perspective” “The Challenges of Translation: A Clinical Perspective” “The Challenges of Translation: A Clinical Perspective”

10 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 10 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 10 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 8:45 PM Jan Nolta 8:45 PM Jan Nolta 8:45 PM Jan Nolta University of California, Davis University of California, Davis University of California, Davis Davis, CA - USA Davis, CA - USA Davis, CA - USA “Working toward cellular therapies to treat Huntington's disease” “Working toward cellular therapies to treat Huntington's disease” “Working toward cellular therapies to treat Huntington's disease”

SATURDAY – DECEMBER 10, 2011 SATURDAY – DECEMBER 10, 2011 SATURDAY – DECEMBER 10, 2011

Session Five: 8:15 AM Session Five: 8:15 AM Session Five: 8:15 AM ISN Symposium on Neurochemistry and Neurobiology of Repair ISN Symposium on Neurochemistry and Neurobiology of Repair ISN Symposium on Neurochemistry and Neurobiology of Repair

8:15 AM Chair: Jacqueline Bresnahan 8:15 AM Chair: Jacqueline Bresnahan 8:15 AM Chair: Jacqueline Bresnahan University of California, San Francisco University of California, San Francisco University of California, San Francisco San Francisco, CA - USA San Francisco, CA - USA San Francisco, CA - USA

8:30 AM Linda Noble -Haeusslein 8:30 AM Linda Noble -Haeusslein 8:30 AM Linda Noble -Haeusslein University of California, San Francisco University of California, San Francisco University of California, San Francisco San Francisco, CA - USA San Francisco, CA - USA San Francisco, CA - USA “Matrix metalloproteinases as modifiers of injury and recovery processes after “Matrix metalloproteinases as modifiers of injury and recovery processes after “Matrix metalloproteinases as modifiers of injury and recovery processes after spinal cord injury” spinal cord injury” spinal cord injury”

9:00 AM Herb Geller 9:00 AM Herb Geller 9:00 AM Herb Geller NIH/NHLBI NIH/NHLBI NIH/NHLBI Bethesda, MD - USA Bethesda, MD - USA Bethesda, MD - USA “The Sour Side of Sugars: Chondroitin Sulfate Signaling in Axonal Guidance” “The Sour Side of Sugars: Chondroitin Sulfate Signaling in Axonal Guidance” “The Sour Side of Sugars: Chondroitin Sulfate Signaling in Axonal Guidance”

9:30 AM Roman Giger 9:30 AM Roman Giger 9:30 AM Roman Giger University of Michigan University of Michigan University of Michigan Ann Arbor, MI - USA Ann Arbor, MI - USA Ann Arbor, MI - USA “Identification and functional characterization of novel receptors for inhibitory “Identification and functional characterization of novel receptors for inhibitory “Identification and functional characterization of novel receptors for inhibitory chondroitin sulfate proteoglycans.” chondroitin sulfate proteoglycans.” chondroitin sulfate proteoglycans.”

10:00 AM Klaus Nave 10:00 AM Klaus Nave 10:00 AM Klaus Nave Max Planck Institute for Experimental Medicine – Germany Max Planck Institute for Experimental Medicine – Germany Max Planck Institute for Experimental Medicine – Germany “The role of myelinating glia in preserving axon function” “The role of myelinating glia in preserving axon function” “The role of myelinating glia in preserving axon function”

10:30 AM BREAK 10:30 AM BREAK 10:30 AM BREAK

11:00 AM Featured Speaker 11:00 AM Featured Speaker 11:00 AM Featured Speaker Ed Boyden Ed Boyden Ed Boyden Massachusetts Institute of Technology Massachusetts Institute of Technology Massachusetts Institute of Technology Cambridge, MA - USA Cambridge, MA - USA Cambridge, MA - USA “Optogenetics: Tools for Controlling Brain Circuits With Light” “Optogenetics: Tools for Controlling Brain Circuits With Light” “Optogenetics: Tools for Controlling Brain Circuits With Light”

12:00 Noon LUNCH 12:00 Noon LUNCH 12:00 Noon LUNCH

1:00 PM Viewing: Poster Session 2 1:00 PM Viewing: Poster Session 2 1:00 PM Viewing: Poster Session 2

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 11 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 11 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 11 Session Six: 4:15 PM – 6:00 PM Session Six: 4:15 PM – 6:00 PM Session Six: 4:15 PM – 6:00 PM Route 28 Summit Presentations – Novel ways to exploit stem cells for recovery of CNS function. Route 28 Summit Presentations – Novel ways to exploit stem cells for recovery of CNS function. Route 28 Summit Presentations – Novel ways to exploit stem cells for recovery of CNS function.

4:15 PM Chair: Theo Palmer 4:15 PM Chair: Theo Palmer 4:15 PM Chair: Theo Palmer Stanford University Stanford University Stanford University Palo Alto, CA - USA Palo Alto, CA - USA Palo Alto, CA - USA

Symposium Summary: James Guest and John Steeves Symposium Summary: James Guest and John Steeves Symposium Summary: James Guest and John Steeves

6:30 PM Symposium Banquet 6:30 PM Symposium Banquet 6:30 PM Symposium Banquet

7:30 PM Awards Presentation (Banquet Hall) 7:30 PM Awards Presentation (Banquet Hall) 7:30 PM Awards Presentation (Banquet Hall)

SUNDAY – DECEMBER 11, 2011 SUNDAY – DECEMBER 11, 2011 SUNDAY – DECEMBER 11, 2011

Departure of Participants Departure of Participants Departure of Participants

12 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 12 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 12 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS

O-1 Sprouting, Regeneration and Relay distinct and intriguing mechanisms for O-1 Sprouting, Regeneration and Relay distinct and intriguing mechanisms for O-1 Sprouting, Regeneration and Relay distinct and intriguing mechanisms for Formation After SCI: Realistic Targets for enhancing outcomes after spinal cord injury. Formation After SCI: Realistic Targets for enhancing outcomes after spinal cord injury. Formation After SCI: Realistic Targets for enhancing outcomes after spinal cord injury. Translation? The translational relevance of these approaches Translation? The translational relevance of these approaches Translation? The translational relevance of these approaches will be discussed. will be discussed. will be discussed. M. Tuszynski1,2, P. Lu1, E. Rosenzweig1, L. M. Tuszynski1,2, P. Lu1, E. Rosenzweig1, L. M. Tuszynski1,2, P. Lu1, E. Rosenzweig1, L. Alto1, K. Kadoya1, A. Blesch1, J. Brock1, L. Alto1, K. Kadoya1, A. Blesch1, J. Brock1, L. Alto1, K. Kadoya1, A. Blesch1, J. Brock1, L. Havton3, M. Beattie4, R. Edgerton5, G. O-2 Out Of The Frying Pan Into The Fire Havton3, M. Beattie4, R. Edgerton5, G. O-2 Out Of The Frying Pan Into The Fire Havton3, M. Beattie4, R. Edgerton5, G. O-2 Out Of The Frying Pan Into The Fire Courtine6, J. Bresnahan4 - BCI Faces Real World Application Courtine6, J. Bresnahan4 - BCI Faces Real World Application Courtine6, J. Bresnahan4 - BCI Faces Real World Application 1University of California – San Diego, 1University of California – San Diego, 1University of California – San Diego, 2Veterans Administration Medical Center – La A. Kubler 2Veterans Administration Medical Center – La A. Kubler 2Veterans Administration Medical Center – La A. Kubler Jolla, 3University of California-Irvine, Department of Psychology, University of Jolla, 3University of California-Irvine, Department of Psychology, University of Jolla, 3University of California-Irvine, Department of Psychology, University of 4University of California – San Francisco, Wuerzburg, Germany 4University of California – San Francisco, Wuerzburg, Germany 4University of California – San Francisco, Wuerzburg, Germany 5University of California –Los Angeles, 5University of California –Los Angeles, 5University of California –Los Angeles, 6University of Zurich Brain-Computer Interfaces (BCIs) have 6University of Zurich Brain-Computer Interfaces (BCIs) have 6University of Zurich Brain-Computer Interfaces (BCIs) have been investigated for more than 20 years. Many been investigated for more than 20 years. Many been investigated for more than 20 years. Many Substantial progress has been made in the BCIs use non-invasive electroencephalography Substantial progress has been made in the BCIs use non-invasive electroencephalography Substantial progress has been made in the BCIs use non-invasive electroencephalography last 30 years in understanding fundamental as a measurement technique and mostly last 30 years in understanding fundamental as a measurement technique and mostly last 30 years in understanding fundamental as a measurement technique and mostly responses of the nervous system to injury, and sensorimotor rhythms (SMR) or event related responses of the nervous system to injury, and sensorimotor rhythms (SMR) or event related responses of the nervous system to injury, and sensorimotor rhythms (SMR) or event related in elucidating mechanisms limiting central potentials (e.g., P300) as an input signal. Since in elucidating mechanisms limiting central potentials (e.g., P300) as an input signal. Since in elucidating mechanisms limiting central potentials (e.g., P300) as an input signal. Since axonal regeneration. Accordingly, different the early days of BCI in the late 1980’s not only axonal regeneration. Accordingly, different the early days of BCI in the late 1980’s not only axonal regeneration. Accordingly, different the early days of BCI in the late 1980’s not only experimental approaches target different aspects data processing has improved, but also stimuli experimental approaches target different aspects data processing has improved, but also stimuli experimental approaches target different aspects data processing has improved, but also stimuli of the degenerative/regenerative response. Some presentation, feedback modes and training of the degenerative/regenerative response. Some presentation, feedback modes and training of the degenerative/regenerative response. Some presentation, feedback modes and training therapeutic discovery efforts aim to minimize protocols have been varied and a plethora of therapeutic discovery efforts aim to minimize protocols have been varied and a plethora of therapeutic discovery efforts aim to minimize protocols have been varied and a plethora of the early effects of injury and to reduce applications have been developed and refined. the early effects of injury and to reduce applications have been developed and refined. the early effects of injury and to reduce applications have been developed and refined. secondary injury (neuroprotection). Other These applications are facing the challenge of secondary injury (neuroprotection). Other These applications are facing the challenge of secondary injury (neuroprotection). Other These applications are facing the challenge of efforts focus on improving the nervous system’s being transferred from the research laboratory efforts focus on improving the nervous system’s being transferred from the research laboratory efforts focus on improving the nervous system’s being transferred from the research laboratory ability to recover from injury, targeting either: into real life situations to serve motor-impaired ability to recover from injury, targeting either: into real life situations to serve motor-impaired ability to recover from injury, targeting either: into real life situations to serve motor-impaired 1) enhancement of functional reorganization of people in their homes as assistive technology. 1) enhancement of functional reorganization of people in their homes as assistive technology. 1) enhancement of functional reorganization of people in their homes as assistive technology. the nervous system (e.g., through rehabilitation Evaluation studies are carried out at the the nervous system (e.g., through rehabilitation Evaluation studies are carried out at the the nervous system (e.g., through rehabilitation Evaluation studies are carried out at the or electrical stimulation), 2) post-injury patients’ bedside and their home environment. or electrical stimulation), 2) post-injury patients’ bedside and their home environment. or electrical stimulation), 2) post-injury patients’ bedside and their home environment. pharmacological modulation of spinal Recently BCI control was integrated into pharmacological modulation of spinal Recently BCI control was integrated into pharmacological modulation of spinal Recently BCI control was integrated into neurotransmitter systems, 3) enhancement of commercial assistive technology ICT product neurotransmitter systems, 3) enhancement of commercial assistive technology ICT product neurotransmitter systems, 3) enhancement of commercial assistive technology ICT product intraspinal compensatory collateral sprouting, 4) and the usability of the first prototype was intraspinal compensatory collateral sprouting, 4) and the usability of the first prototype was intraspinal compensatory collateral sprouting, 4) and the usability of the first prototype was promotion of true axonal regeneration into and evaluated in terms of effectiveness, efficiency promotion of true axonal regeneration into and evaluated in terms of effectiveness, efficiency promotion of true axonal regeneration into and evaluated in terms of effectiveness, efficiency beyond a lesion cavity, and 5) formation of and user satisfaction. High performance with the beyond a lesion cavity, and 5) formation of and user satisfaction. High performance with the beyond a lesion cavity, and 5) formation of and user satisfaction. High performance with the novel circuitry across a lesion site, i.e., neuronal BCI and high overall satisfaction of users and novel circuitry across a lesion site, i.e., neuronal BCI and high overall satisfaction of users and novel circuitry across a lesion site, i.e., neuronal BCI and high overall satisfaction of users and relay formation. Several of these approaches AT-experts, contrast with the fact that none of relay formation. Several of these approaches AT-experts, contrast with the fact that none of relay formation. Several of these approaches AT-experts, contrast with the fact that none of overlap; for example, rehabilitation or electrical them could imagine the use of the device in overlap; for example, rehabilitation or electrical them could imagine the use of the device in overlap; for example, rehabilitation or electrical them could imagine the use of the device in stimulation can modulate transmitter systems daily life without improvements. However, an stimulation can modulate transmitter systems daily life without improvements. However, an stimulation can modulate transmitter systems daily life without improvements. However, an and axonal sprouting. increasingly better understanding of the factors and axonal sprouting. increasingly better understanding of the factors and axonal sprouting. increasingly better understanding of the factors This talk will provide an update on SCI influencing BCI performance renders such This talk will provide an update on SCI influencing BCI performance renders such This talk will provide an update on SCI influencing BCI performance renders such research that focuses on structural aspects of improvement likely in the near future. research that focuses on structural aspects of improvement likely in the near future. research that focuses on structural aspects of improvement likely in the near future. neural repair. We will attempt to demonstrate neural repair. We will attempt to demonstrate neural repair. We will attempt to demonstrate that enhancement of endogenous sprouting, O-3 Micro-Electrodes In And On The that enhancement of endogenous sprouting, O-3 Micro-Electrodes In And On The that enhancement of endogenous sprouting, O-3 Micro-Electrodes In And On The induction of bridging axonal regeneration, and Cerebral Cortex For Decoding And Encoding induction of bridging axonal regeneration, and Cerebral Cortex For Decoding And Encoding induction of bridging axonal regeneration, and Cerebral Cortex For Decoding And Encoding formation of novel relay circuits all constitute Information formation of novel relay circuits all constitute Information formation of novel relay circuits all constitute Information

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 13 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 13 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 13 ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS

B. Greger B. Greger B. Greger Department of Bioengineering, Brain-machine interfaces (BMI) and Department of Bioengineering, Brain-machine interfaces (BMI) and Department of Bioengineering, Brain-machine interfaces (BMI) and University of Utah, Biomedical Polymers neuroprosthetic technology have the potential to University of Utah, Biomedical Polymers neuroprosthetic technology have the potential to University of Utah, Biomedical Polymers neuroprosthetic technology have the potential to Research Building, 20 South 2030 East, Salt dramatically improve quality of life after Research Building, 20 South 2030 East, Salt dramatically improve quality of life after Research Building, 20 South 2030 East, Salt dramatically improve quality of life after Lake City, UT 84112-9458 paralysis resulting from spinal cord injury, Lake City, UT 84112-9458 paralysis resulting from spinal cord injury, Lake City, UT 84112-9458 paralysis resulting from spinal cord injury, stroke or traumatic brain injury. We have stroke or traumatic brain injury. We have stroke or traumatic brain injury. We have We are investigating the ability of recently demonstrated that brain activity can be We are investigating the ability of recently demonstrated that brain activity can be We are investigating the ability of recently demonstrated that brain activity can be micro-ECoG grids to record multiple used to control Functional Electrical Stimulation micro-ECoG grids to record multiple used to control Functional Electrical Stimulation micro-ECoG grids to record multiple used to control Functional Electrical Stimulation independent neural signals from the cortical (FES) delivered to muscles and reanimate independent neural signals from the cortical (FES) delivered to muscles and reanimate independent neural signals from the cortical (FES) delivered to muscles and reanimate surface for use in neural prosthetic applications. simple movements of an otherwise paralyzed surface for use in neural prosthetic applications. simple movements of an otherwise paralyzed surface for use in neural prosthetic applications. simple movements of an otherwise paralyzed This study describes the classification of spoken wrist1. Monkeys rapidly learned to modulate the This study describes the classification of spoken wrist1. Monkeys rapidly learned to modulate the This study describes the classification of spoken wrist1. Monkeys rapidly learned to modulate the words using surface local field potentials (LFPs) activity of individual neurons in motor areas of words using surface local field potentials (LFPs) activity of individual neurons in motor areas of words using surface local field potentials (LFPs) activity of individual neurons in motor areas of recorded on subdural micro-ECoG grids. Data the brain in order to control the timing and recorded on subdural micro-ECoG grids. Data the brain in order to control the timing and recorded on subdural micro-ECoG grids. Data the brain in order to control the timing and recorded from these micro-ECoG grids magnitude of FES delivered to temporarily recorded from these micro-ECoG grids magnitude of FES delivered to temporarily recorded from these micro-ECoG grids magnitude of FES delivered to temporarily supported accurate and rapid classification of paralyzed wrist muscles. In addition to direct supported accurate and rapid classification of paralyzed wrist muscles. In addition to direct supported accurate and rapid classification of paralyzed wrist muscles. In addition to direct spoken words. Furthermore, electrodes spaced muscle stimulation, another promising spoken words. Furthermore, electrodes spaced muscle stimulation, another promising spoken words. Furthermore, electrodes spaced muscle stimulation, another promising only millimeters apart demonstrated varying neuroprosthetic approach is intraspinal only millimeters apart demonstrated varying neuroprosthetic approach is intraspinal only millimeters apart demonstrated varying neuroprosthetic approach is intraspinal classification characteristics and strong stimulation. This technique has shown promise classification characteristics and strong stimulation. This technique has shown promise classification characteristics and strong stimulation. This technique has shown promise correlations with different words, suggesting in the lumbar spinal cord with success in correlations with different words, suggesting in the lumbar spinal cord with success in correlations with different words, suggesting in the lumbar spinal cord with success in that cortical surface LFPs may encoded reanimating coordinated lower extremity that cortical surface LFPs may encoded reanimating coordinated lower extremity that cortical surface LFPs may encoded reanimating coordinated lower extremity information with high temporal and spatial movements, including weight bearing and information with high temporal and spatial movements, including weight bearing and information with high temporal and spatial movements, including weight bearing and resolution. Arrays which penetrate into the stepping in animal models. We recently resolution. Arrays which penetrate into the stepping in animal models. We recently resolution. Arrays which penetrate into the stepping in animal models. We recently parenchymal of the brain are being used by quantified the hand and arm movements evoked parenchymal of the brain are being used by quantified the hand and arm movements evoked parenchymal of the brain are being used by quantified the hand and arm movements evoked several groups to provide control signals for by cervical spinal stimulation2. Movements of several groups to provide control signals for by cervical spinal stimulation2. Movements of several groups to provide control signals for by cervical spinal stimulation2. Movements of neural prosthetic applications. We have also the digits, wrist and arm were readily evoked by neural prosthetic applications. We have also the digits, wrist and arm were readily evoked by neural prosthetic applications. We have also the digits, wrist and arm were readily evoked by been investing these devices focusing on fine intraspinal stimulation in the cervical cord of been investing these devices focusing on fine intraspinal stimulation in the cervical cord of been investing these devices focusing on fine intraspinal stimulation in the cervical cord of finger movements and providing sensory sedated monkeys. Due to the ease of activating finger movements and providing sensory sedated monkeys. Due to the ease of activating finger movements and providing sensory sedated monkeys. Due to the ease of activating information through micro-stimulation. Using complex functional movements from a small information through micro-stimulation. Using complex functional movements from a small information through micro-stimulation. Using complex functional movements from a small neural signals recorded from primary motor number of stimulating sites, intraspinal neural signals recorded from primary motor number of stimulating sites, intraspinal neural signals recorded from primary motor number of stimulating sites, intraspinal cortex we have been able to classify individual stimulation may be an ideal method for cortex we have been able to classify individual stimulation may be an ideal method for cortex we have been able to classify individual stimulation may be an ideal method for finger movements with a high degree of success. reanimating paralyzed limbs under direct finger movements with a high degree of success. reanimating paralyzed limbs under direct finger movements with a high degree of success. reanimating paralyzed limbs under direct We've been able to evoke subjective perceptions control of a BMI. In addition to directly We've been able to evoke subjective perceptions control of a BMI. In addition to directly We've been able to evoke subjective perceptions control of a BMI. In addition to directly using micro-stimulation. These results further restoring movements, brain-triggered spinal using micro-stimulation. These results further restoring movements, brain-triggered spinal using micro-stimulation. These results further restoring movements, brain-triggered spinal support the micro-electrode technology as a stimulation may also aid in guiding recovery support the micro-electrode technology as a stimulation may also aid in guiding recovery support the micro-electrode technology as a stimulation may also aid in guiding recovery promising technology for both motor and and promoting regeneration after injury to the promising technology for both motor and and promoting regeneration after injury to the promising technology for both motor and and promoting regeneration after injury to the sensory neural prosthetic applications. brain or spinal cord. Recent work demonstrated sensory neural prosthetic applications. brain or spinal cord. Recent work demonstrated sensory neural prosthetic applications. brain or spinal cord. Recent work demonstrated that paring activity recorded within the brain that paring activity recorded within the brain that paring activity recorded within the brain O-4 Leveraging Neural Plasticity For The with stimulation delivered a short distance away O-4 Leveraging Neural Plasticity For The with stimulation delivered a short distance away O-4 Leveraging Neural Plasticity For The with stimulation delivered a short distance away Treatment Of Paralysis And Other lead to durable increases in connectivity based Treatment Of Paralysis And Other lead to durable increases in connectivity based Treatment Of Paralysis And Other lead to durable increases in connectivity based Movement Disorders on Hebbian mechanisms. We are currently Movement Disorders on Hebbian mechanisms. We are currently Movement Disorders on Hebbian mechanisms. We are currently testing whether synchronizing brain activity testing whether synchronizing brain activity testing whether synchronizing brain activity C. T. Moritz with intraspinal stimulation below an C. T. Moritz with intraspinal stimulation below an C. T. Moritz with intraspinal stimulation below an Departments of Rehabilitation Medicine incomplete spinal lesion leads to functional Departments of Rehabilitation Medicine incomplete spinal lesion leads to functional Departments of Rehabilitation Medicine incomplete spinal lesion leads to functional and Physiology & Biophysics, University of recovery. Such a regenerating BMI may have and Physiology & Biophysics, University of recovery. Such a regenerating BMI may have and Physiology & Biophysics, University of recovery. Such a regenerating BMI may have Washington School of Medicine, Seattle, WA, the capacity to direct synaptic strength in spared Washington School of Medicine, Seattle, WA, the capacity to direct synaptic strength in spared Washington School of Medicine, Seattle, WA, the capacity to direct synaptic strength in spared USA 98195 USA 98195 USA 98195

14 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 14 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 14 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS pathways, either alone or in collaboration with to bring the product to market. In this talk, I pathways, either alone or in collaboration with to bring the product to market. In this talk, I pathways, either alone or in collaboration with to bring the product to market. In this talk, I stem cell therapies. will discuss the progress that has been made in stem cell therapies. will discuss the progress that has been made in stem cell therapies. will discuss the progress that has been made in References motor-based BCI research as well as perceived References motor-based BCI research as well as perceived References motor-based BCI research as well as perceived 1. Moritz, C. T.* , Perlmutter, S. I., Fetz, E. E. (2008) and real limitations to translating this 1. Moritz, C. T.* , Perlmutter, S. I., Fetz, E. E. (2008) and real limitations to translating this 1. Moritz, C. T.* , Perlmutter, S. I., Fetz, E. E. (2008) and real limitations to translating this Direct control of paralyzed muscles by cortical Direct control of paralyzed muscles by cortical Direct control of paralyzed muscles by cortical neurons. Nature, 456, 639-642. technology to the clinic. The consumer neurons. Nature, 456, 639-642. technology to the clinic. The consumer neurons. Nature, 456, 639-642. technology to the clinic. The consumer 2. Moritz, C. T.* , Lucas, T. H., Perlmutter, S. I., Fetz, population should be included as an important 2. Moritz, C. T.* , Lucas, T. H., Perlmutter, S. I., Fetz, population should be included as an important 2. Moritz, C. T.* , Lucas, T. H., Perlmutter, S. I., Fetz, population should be included as an important E. E. (2007) Forelimb movements and muscle responses contributor to the development process. In a E. E. (2007) Forelimb movements and muscle responses contributor to the development process. In a E. E. (2007) Forelimb movements and muscle responses contributor to the development process. In a evoked by microstimulation of cervical spinal cord in recent survey of veterans with spinal cord evoked by microstimulation of cervical spinal cord in recent survey of veterans with spinal cord evoked by microstimulation of cervical spinal cord in recent survey of veterans with spinal cord sedated monkeys. Journal of Neurophysiology, 97(1), injury, we found that restoration of sedated monkeys. Journal of Neurophysiology, 97(1), injury, we found that restoration of sedated monkeys. Journal of Neurophysiology, 97(1), injury, we found that restoration of 110-120. 110-120. 110-120. Supported by a National Institutes of Health EUREKA bladder/bowel function and walking ability were Supported by a National Institutes of Health EUREKA bladder/bowel function and walking ability were Supported by a National Institutes of Health EUREKA bladder/bowel function and walking ability were Award (NIH/NINDS 1R01NS066357) and Ruth L. important priorities of the entire group. For Award (NIH/NINDS 1R01NS066357) and Ruth L. important priorities of the entire group. For Award (NIH/NINDS 1R01NS066357) and Ruth L. important priorities of the entire group. For Kirschstein NRSA (NIH/NINDS F32NS5101), an those with tetraplegia, restoration of arm and Kirschstein NRSA (NIH/NINDS F32NS5101), an those with tetraplegia, restoration of arm and Kirschstein NRSA (NIH/NINDS F32NS5101), an those with tetraplegia, restoration of arm and American Heart & Stroke Association Scientist hand function was the most important. Clearly American Heart & Stroke Association Scientist hand function was the most important. Clearly American Heart & Stroke Association Scientist hand function was the most important. Clearly Development Grant (AHA 09SDG2230091), the integration of BCI and other technologies, such Development Grant (AHA 09SDG2230091), the integration of BCI and other technologies, such Development Grant (AHA 09SDG2230091), the integration of BCI and other technologies, such University of Washington Royalty Research Fund University of Washington Royalty Research Fund University of Washington Royalty Research Fund (#4417), and the Bayley Family Foundation, and an NSF as functional electrical stimulation, will be (#4417), and the Bayley Family Foundation, and an NSF as functional electrical stimulation, will be (#4417), and the Bayley Family Foundation, and an NSF as functional electrical stimulation, will be ERC in Sensorimotor Neural Engineering (EEC- critical to delivering a product that meets the ERC in Sensorimotor Neural Engineering (EEC- critical to delivering a product that meets the ERC in Sensorimotor Neural Engineering (EEC- critical to delivering a product that meets the 1028725). priorities of the end users. Independent 1028725). priorities of the end users. Independent 1028725). priorities of the end users. Independent operation was reported to be the most important operation was reported to be the most important operation was reported to be the most important O-5 Is BCI Technology Ready For Prime BCI design characteristic and training time was O-5 Is BCI Technology Ready For Prime BCI design characteristic and training time was O-5 Is BCI Technology Ready For Prime BCI design characteristic and training time was Time? The Science Is Mature And The the least important. Interestingly, even though Time? The Science Is Mature And The the least important. Interestingly, even though Time? The Science Is Mature And The the least important. Interestingly, even though Consumers Are Willing- What Are We more than 70% of respondents indicated that Consumers Are Willing- What Are We more than 70% of respondents indicated that Consumers Are Willing- What Are We more than 70% of respondents indicated that Waiting For? non-invasiveness was a very important design Waiting For? non-invasiveness was a very important design Waiting For? non-invasiveness was a very important design characteristic, more than half indicated that they characteristic, more than half indicated that they characteristic, more than half indicated that they J.L. Collinger would definitely, or very likely, consider having J.L. Collinger would definitely, or very likely, consider having J.L. Collinger would definitely, or very likely, consider having Human Engineering Research surgery to implant BCI electrodes. Individuals Human Engineering Research surgery to implant BCI electrodes. Individuals Human Engineering Research surgery to implant BCI electrodes. Individuals Laboratories, Department of Veterans Affairs, with other disabilities will likely have different Laboratories, Department of Veterans Affairs, with other disabilities will likely have different Laboratories, Department of Veterans Affairs, with other disabilities will likely have different Pittsburgh, PA; Department of Physical priorities and should also be included in pre- Pittsburgh, PA; Department of Physical priorities and should also be included in pre- Pittsburgh, PA; Department of Physical priorities and should also be included in pre- Medicine and Rehabilitation, University of market technology development. Medicine and Rehabilitation, University of market technology development. Medicine and Rehabilitation, University of market technology development. Pittsburgh, Pittsburgh, PA Disclaimer: The views expressed herein are those of the Pittsburgh, Pittsburgh, PA Disclaimer: The views expressed herein are those of the Pittsburgh, Pittsburgh, PA Disclaimer: The views expressed herein are those of the authors and do not reflect the official policy or position of authors and do not reflect the official policy or position of authors and do not reflect the official policy or position of the Department of Veterans Affairs, Department of the the Department of Veterans Affairs, Department of the the Department of Veterans Affairs, Department of the Brain-computer interface (BCI) Army, Department of Defense, or the United States Brain-computer interface (BCI) Army, Department of Defense, or the United States Brain-computer interface (BCI) Army, Department of Defense, or the United States technology can take many forms but all have the government. technology can take many forms but all have the government. technology can take many forms but all have the government. same goal of translating command signals from same goal of translating command signals from same goal of translating command signals from the brain to functional control signals for an O-6 The Role of Neural Prosthesis and the brain to functional control signals for an O-6 The Role of Neural Prosthesis and the brain to functional control signals for an O-6 The Role of Neural Prosthesis and external device. Researchers have been Neural Stimulation in the Restoration of external device. Researchers have been Neural Stimulation in the Restoration of external device. Researchers have been Neural Stimulation in the Restoration of successful in developing and testing BCI Function successful in developing and testing BCI Function successful in developing and testing BCI Function systems to control spellers, computer cursors, systems to control spellers, computer cursors, systems to control spellers, computer cursors, and even robotic arms. Much of this research P. H. Peckham and even robotic arms. Much of this research P. H. Peckham and even robotic arms. Much of this research P. H. Peckham has been conducted in non-human primates or Case Western Reserve University and has been conducted in non-human primates or Case Western Reserve University and has been conducted in non-human primates or Case Western Reserve University and with able-bodied individuals. Potential Veterans Affairs Medical Center, Cleveland, with able-bodied individuals. Potential Veterans Affairs Medical Center, Cleveland, with able-bodied individuals. Potential Veterans Affairs Medical Center, Cleveland, consumers of BCI technology are eager to take OH consumers of BCI technology are eager to take OH consumers of BCI technology are eager to take OH advantage of this technology to assist with advantage of this technology to assist with advantage of this technology to assist with activities of daily living and improve their Major advances have been made over activities of daily living and improve their Major advances have been made over activities of daily living and improve their Major advances have been made over quality of life. Each type of BCI system has the past decade in use of neuroprostheses for quality of life. Each type of BCI system has the past decade in use of neuroprostheses for quality of life. Each type of BCI system has the past decade in use of neuroprostheses for advantages and disadvantages, as well as unique restoration of motor function. These advances advantages and disadvantages, as well as unique restoration of motor function. These advances advantages and disadvantages, as well as unique restoration of motor function. These advances scientific, technical, and regulatory challenges have been built on the fundamental science of scientific, technical, and regulatory challenges have been built on the fundamental science of scientific, technical, and regulatory challenges have been built on the fundamental science of

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 15 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 15 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 15 ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS neural excitation and the technologies for generally in the extracellular spaces, for neural excitation and the technologies for generally in the extracellular spaces, for neural excitation and the technologies for generally in the extracellular spaces, for implantable stimulation and control. The minutes, hours, even days. A host of basic implantable stimulation and control. The minutes, hours, even days. A host of basic implantable stimulation and control. The minutes, hours, even days. A host of basic technologies have advanced to provide behaviours such as the cell cycle, cell division, technologies have advanced to provide behaviours such as the cell cycle, cell division, technologies have advanced to provide behaviours such as the cell cycle, cell division, operational systems that function in the human cell shape, cell migration and cell growth may operational systems that function in the human cell shape, cell migration and cell growth may operational systems that function in the human cell shape, cell migration and cell growth may body for decades, and include implantable all be controlled by these small electrical signals body for decades, and include implantable all be controlled by these small electrical signals body for decades, and include implantable all be controlled by these small electrical signals electrodes, stimulation devices, and sensors. during normal development. electrodes, stimulation devices, and sensors. during normal development. electrodes, stimulation devices, and sensors. during normal development. The neural interface between the excitable tissue Following damage in several systems, The neural interface between the excitable tissue Following damage in several systems, The neural interface between the excitable tissue Following damage in several systems, and the delivery electrode are enabling steady electrical signals rapidly re-appear and and the delivery electrode are enabling steady electrical signals rapidly re-appear and and the delivery electrode are enabling steady electrical signals rapidly re-appear and evermore powerful control and precision in the again seem to regulate a range of coordinated evermore powerful control and precision in the again seem to regulate a range of coordinated evermore powerful control and precision in the again seem to regulate a range of coordinated delivery of stimulation, not only providing for cell activities. In epithelial tissues such as skin delivery of stimulation, not only providing for cell activities. In epithelial tissues such as skin delivery of stimulation, not only providing for cell activities. In epithelial tissues such as skin excitation but also blocking of neural activity and cornea, there is direct evidence for electrical excitation but also blocking of neural activity and cornea, there is direct evidence for electrical excitation but also blocking of neural activity and cornea, there is direct evidence for electrical (e.g. for annihilation of pain or spasticity) and regulation of the axis of cell division, the rate of (e.g. for annihilation of pain or spasticity) and regulation of the axis of cell division, the rate of (e.g. for annihilation of pain or spasticity) and regulation of the axis of cell division, the rate of selective stimulation. Distributed implantable cell proliferation and the direction of cell selective stimulation. Distributed implantable cell proliferation and the direction of cell selective stimulation. Distributed implantable cell proliferation and the direction of cell systems and brain control interfaces are migration. These events need to be coordinated systems and brain control interfaces are migration. These events need to be coordinated systems and brain control interfaces are migration. These events need to be coordinated currently in development that will provide for successful wound healing. Since there is currently in development that will provide for successful wound healing. Since there is currently in development that will provide for successful wound healing. Since there is greater flexibility in implementation and evidence that these electrical signals may be the greater flexibility in implementation and evidence that these electrical signals may be the greater flexibility in implementation and evidence that these electrical signals may be the performance. earliest to appear at a wound and that they may performance. earliest to appear at a wound and that they may performance. earliest to appear at a wound and that they may The clinical manifestations of these override coexisting chemical signals, they could The clinical manifestations of these override coexisting chemical signals, they could The clinical manifestations of these override coexisting chemical signals, they could findings are the availability of systems that have act as a master regulator signal to kick start an findings are the availability of systems that have act as a master regulator signal to kick start an findings are the availability of systems that have act as a master regulator signal to kick start an been created, and are being developed, to integrated array of coordinated cell behaviours. been created, and are being developed, to integrated array of coordinated cell behaviours. been created, and are being developed, to integrated array of coordinated cell behaviours. restore function. These include many areas of Similar electrical signals have been measured restore function. These include many areas of Similar electrical signals have been measured restore function. These include many areas of Similar electrical signals have been measured the body for people with spinal cord injury, following injury to the central nervous system the body for people with spinal cord injury, following injury to the central nervous system the body for people with spinal cord injury, following injury to the central nervous system including hand grasp, standing and walking, and spinal cord. The mechanisms underlying the including hand grasp, standing and walking, and spinal cord. The mechanisms underlying the including hand grasp, standing and walking, and spinal cord. The mechanisms underlying the breathing, and bladder and bowel control. generation of these signals and the varying breathing, and bladder and bowel control. generation of these signals and the varying breathing, and bladder and bowel control. generation of these signals and the varying Several patients have benefited from systems mechanisms by which electrical signals direct Several patients have benefited from systems mechanisms by which electrical signals direct Several patients have benefited from systems mechanisms by which electrical signals direct that enable more than one function (e.g. hand neuronal cell division, neuronal and glial cell that enable more than one function (e.g. hand neuronal cell division, neuronal and glial cell that enable more than one function (e.g. hand neuronal cell division, neuronal and glial cell function and bladder control). The presentation migration, nerve guidance and epithelial cell function and bladder control). The presentation migration, nerve guidance and epithelial cell function and bladder control). The presentation migration, nerve guidance and epithelial cell will provide examples of both upper and lower migration will be explored. will provide examples of both upper and lower migration will be explored. will provide examples of both upper and lower migration will be explored. extremity neuroprostheses to restore full arm Background References extremity neuroprostheses to restore full arm Background References extremity neuroprostheses to restore full arm Background References mobility and levels of standing and ambulation. McCaig, C.D. Rajnicek, A.M., Song, B. Song, B.& Zhao, mobility and levels of standing and ambulation. McCaig, C.D. Rajnicek, A.M., Song, B. Song, B.& Zhao, mobility and levels of standing and ambulation. McCaig, C.D. Rajnicek, A.M., Song, B. Song, B.& Zhao, M. (2005). Controlling cell behaviour electrically: Current M. (2005). Controlling cell behaviour electrically: Current M. (2005). Controlling cell behaviour electrically: Current Several areas where future advances are likely views and future potential. Physiological Reviews 85, Several areas where future advances are likely views and future potential. Physiological Reviews 85, Several areas where future advances are likely views and future potential. Physiological Reviews 85, to meet clinical challenges will be discussed. 943-978. to meet clinical challenges will be discussed. 943-978. to meet clinical challenges will be discussed. 943-978.

O-7 Electrical signals control multiple cell Zhao, M., Song, B., Pu, J., Wada, T., Reid, B., Tai, G., O-7 Electrical signals control multiple cell Zhao, M., Song, B., Pu, J., Wada, T., Reid, B., Tai, G., O-7 Electrical signals control multiple cell Zhao, M., Song, B., Pu, J., Wada, T., Reid, B., Tai, G., behaviours. Wang, F., Guo, A.,Walczysko, P., Gu, Y., Sasaki, T., behaviours. Wang, F., Guo, A.,Walczysko, P., Gu, Y., Sasaki, T., behaviours. Wang, F., Guo, A.,Walczysko, P., Gu, Y., Sasaki, T., Suzuki, A., Forrester, J.V., Bourne, H., Devreotes, P., Suzuki, A., Forrester, J.V., Bourne, H., Devreotes, P., Suzuki, A., Forrester, J.V., Bourne, H., Devreotes, P., McCaig, C.D. & Penninger, J. (2006). Electrical signals McCaig, C.D. & Penninger, J. (2006). Electrical signals McCaig, C.D. & Penninger, J. (2006). Electrical signals C. D. McCaig control wound healing via phosphatidyl –3 kinase  and C. D. McCaig control wound healing via phosphatidyl –3 kinase  and C. D. McCaig control wound healing via phosphatidyl –3 kinase  and University of Aberdeen, Scotland PTEN. Nature 442, 457-460. University of Aberdeen, Scotland PTEN. Nature 442, 457-460. University of Aberdeen, Scotland PTEN. Nature 442, 457-460.

There is a long history of the use of McCaig, C.D., Rajnicek, A.M. & Song, B. (2009). There is a long history of the use of McCaig, C.D., Rajnicek, A.M. & Song, B. (2009). There is a long history of the use of McCaig, C.D., Rajnicek, A.M. & Song, B. (2009). electrical stimulation in medicine. For instance Electrical Dimensions in Cell Science. J. Cell Sc. 122, electrical stimulation in medicine. For instance Electrical Dimensions in Cell Science. J. Cell Sc. 122, electrical stimulation in medicine. For instance Electrical Dimensions in Cell Science. J. Cell Sc. 122, 4267-4276. 4267-4276. 4267-4276. the Romans used the discharge from electrical the Romans used the discharge from electrical the Romans used the discharge from electrical fish to treat a number of pathologies, including O-8 Can Neural Stem Cells be used to fish to treat a number of pathologies, including O-8 Can Neural Stem Cells be used to fish to treat a number of pathologies, including O-8 Can Neural Stem Cells be used to gout and migraine. More recently, we have treat Alzheimer disease? gout and migraine. More recently, we have treat Alzheimer disease? gout and migraine. More recently, we have treat Alzheimer disease? become aware that many tissues generate their become aware that many tissues generate their become aware that many tissues generate their own electrical signals which are present M. Blurton-Jones own electrical signals which are present M. Blurton-Jones own electrical signals which are present M. Blurton-Jones

16 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 16 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 16 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS

Department of Neurobiology & The Spinal Cord Research Center, Department of Neurobiology & The Spinal Cord Research Center, Department of Neurobiology & The Spinal Cord Research Center, Behavior, University of California at Irvine, Department of Neurobiology and Anatomy, Behavior, University of California at Irvine, Department of Neurobiology and Anatomy, Behavior, University of California at Irvine, Department of Neurobiology and Anatomy, Irvine, CA 92697-1705 Drexel University College of Medicine, Irvine, CA 92697-1705 Drexel University College of Medicine, Irvine, CA 92697-1705 Drexel University College of Medicine, Philadelphia, PA 19129 Philadelphia, PA 19129 Philadelphia, PA 19129 Alzheimer disease (AD) is the leading Alzheimer disease (AD) is the leading Alzheimer disease (AD) is the leading cause of age-related dementia, affecting over 5 Spinal cord injury (SCI) is characterized cause of age-related dementia, affecting over 5 Spinal cord injury (SCI) is characterized cause of age-related dementia, affecting over 5 Spinal cord injury (SCI) is characterized million people in the US alone. Unfortunately, by cell death and loss of connectivity resulting million people in the US alone. Unfortunately, by cell death and loss of connectivity resulting million people in the US alone. Unfortunately, by cell death and loss of connectivity resulting currently approved therapies are largely in permanent functional deficits. Transplants of currently approved therapies are largely in permanent functional deficits. Transplants of currently approved therapies are largely in permanent functional deficits. Transplants of palliative. Thus, there is a critical need to neural progenitor cells (NPC) have a potential to palliative. Thus, there is a critical need to neural progenitor cells (NPC) have a potential to palliative. Thus, there is a critical need to neural progenitor cells (NPC) have a potential to identify and test novel approaches to treat this replace neurons and promote connectivity, but identify and test novel approaches to treat this replace neurons and promote connectivity, but identify and test novel approaches to treat this replace neurons and promote connectivity, but disorder. Recently, we examined the effects of significant challenges remain regarding disorder. Recently, we examined the effects of significant challenges remain regarding disorder. Recently, we examined the effects of significant challenges remain regarding neural stem cell (NSC) transplantation in a neuronal integration and functional neural stem cell (NSC) transplantation in a neuronal integration and functional neural stem cell (NSC) transplantation in a neuronal integration and functional transgenic model of AD. Our studies revealed connectivity. To address these issues we transgenic model of AD. Our studies revealed connectivity. To address these issues we transgenic model of AD. Our studies revealed connectivity. To address these issues we that haplotype-matched murine NSCs can developed a relay model of SCI repair where that haplotype-matched murine NSCs can developed a relay model of SCI repair where that haplotype-matched murine NSCs can developed a relay model of SCI repair where improve learning and memory in aged 3xTg-AD graft derived neurons are used to reconnect improve learning and memory in aged 3xTg-AD graft derived neurons are used to reconnect improve learning and memory in aged 3xTg-AD graft derived neurons are used to reconnect mice. Interestingly, NSCs have no effect on the injured dorsal column sensory axons with the mice. Interestingly, NSCs have no effect on the injured dorsal column sensory axons with the mice. Interestingly, NSCs have no effect on the injured dorsal column sensory axons with the underlying beta-amyloid or tangle pathology. denervated dorsal column nuclei (DCN). underlying beta-amyloid or tangle pathology. denervated dorsal column nuclei (DCN). underlying beta-amyloid or tangle pathology. denervated dorsal column nuclei (DCN). Instead, the mechanism underlying improved Neuronal and glial restricted precursors Instead, the mechanism underlying improved Neuronal and glial restricted precursors Instead, the mechanism underlying improved Neuronal and glial restricted precursors cognition involves a robust enhancement of (NRP/GRP), expressing the human placental cognition involves a robust enhancement of (NRP/GRP), expressing the human placental cognition involves a robust enhancement of (NRP/GRP), expressing the human placental hippocampal synaptic connectivity, mediated by alkaline phosphatase (AP) marker, were hippocampal synaptic connectivity, mediated by alkaline phosphatase (AP) marker, were hippocampal synaptic connectivity, mediated by alkaline phosphatase (AP) marker, were brain-derived neurotrophic factor. Although transplanted into a C1 dorsal columns injury. A brain-derived neurotrophic factor. Although transplanted into a C1 dorsal columns injury. A brain-derived neurotrophic factor. Although transplanted into a C1 dorsal columns injury. A these initial findings suggest that NSC week later, BDNF-expressing lentivirus was these initial findings suggest that NSC week later, BDNF-expressing lentivirus was these initial findings suggest that NSC week later, BDNF-expressing lentivirus was transplantation could provide a promising injected into the DCN to guide graft axons to transplantation could provide a promising injected into the DCN to guide graft axons to transplantation could provide a promising injected into the DCN to guide graft axons to therapeutic approach for AD a great deal of the intended target. We used tracing methods therapeutic approach for AD a great deal of the intended target. We used tracing methods therapeutic approach for AD a great deal of the intended target. We used tracing methods additional work is needed. For example, NSC and immunocytochemical analysis by light and additional work is needed. For example, NSC and immunocytochemical analysis by light and additional work is needed. For example, NSC and immunocytochemical analysis by light and transplantation fails to modify the underlying electron microscopy to demonstrate that NRP- transplantation fails to modify the underlying electron microscopy to demonstrate that NRP- transplantation fails to modify the underlying electron microscopy to demonstrate that NRP- beta-amyloid pathology. Long-term efficacy derived neurons are capable of establishing beta-amyloid pathology. Long-term efficacy derived neurons are capable of establishing beta-amyloid pathology. Long-term efficacy derived neurons are capable of establishing may therefore require combinatorial approaches afferent and efferent synaptic connections with may therefore require combinatorial approaches afferent and efferent synaptic connections with may therefore require combinatorial approaches afferent and efferent synaptic connections with that also target beta-amyloid or tangle the injured host at the site of injury and the that also target beta-amyloid or tangle the injured host at the site of injury and the that also target beta-amyloid or tangle the injured host at the site of injury and the pathology. To that end we have begun testing DCN, respectively. Specifically, we observed pathology. To that end we have begun testing DCN, respectively. Specifically, we observed pathology. To that end we have begun testing DCN, respectively. Specifically, we observed the use of NSCs to deliver disease-modifying anterogradely traced sensory axons regenerating the use of NSCs to deliver disease-modifying anterogradely traced sensory axons regenerating the use of NSCs to deliver disease-modifying anterogradely traced sensory axons regenerating proteins such as neprilysin. Our experiments into the graft, and robust growth of graft-derived proteins such as neprilysin. Our experiments into the graft, and robust growth of graft-derived proteins such as neprilysin. Our experiments into the graft, and robust growth of graft-derived reveal that NSC-mediated delivery of neprilysin AP-positive axons along the neurotrophin reveal that NSC-mediated delivery of neprilysin AP-positive axons along the neurotrophin reveal that NSC-mediated delivery of neprilysin AP-positive axons along the neurotrophin can dramatically reduce beta-amyloid pathology gradient into the DCN. We then used stimulus can dramatically reduce beta-amyloid pathology gradient into the DCN. We then used stimulus can dramatically reduce beta-amyloid pathology gradient into the DCN. We then used stimulus in aged 3xTg-AD mice. On-going studies will evoked c-Fos expression to test synaptic activity in aged 3xTg-AD mice. On-going studies will evoked c-Fos expression to test synaptic activity in aged 3xTg-AD mice. On-going studies will evoked c-Fos expression to test synaptic activity determine whether this approach provides and found that host axons formed active determine whether this approach provides and found that host axons formed active determine whether this approach provides and found that host axons formed active additional long-term cognitive benefits. synapses with graft neurons at the injury site. additional long-term cognitive benefits. synapses with graft neurons at the injury site. additional long-term cognitive benefits. synapses with graft neurons at the injury site. Experiments aimed at identifying and testing We also observed reproducible Experiments aimed at identifying and testing We also observed reproducible Experiments aimed at identifying and testing We also observed reproducible candidate human NSCs lines are also being electrophysiological activity in the DCN, with a candidate human NSCs lines are also being electrophysiological activity in the DCN, with a candidate human NSCs lines are also being electrophysiological activity in the DCN, with a actively pursued. temporal delay predicted by the relay model, actively pursued. temporal delay predicted by the relay model, actively pursued. temporal delay predicted by the relay model, providing evidence for the presence of a providing evidence for the presence of a providing evidence for the presence of a O-9 Transplanting neural progenitors to functional synapse at the grafting site and the O-9 Transplanting neural progenitors to functional synapse at the grafting site and the O-9 Transplanting neural progenitors to functional synapse at the grafting site and the reconnect the injured spinal cord conduction of action potentials by graft axons to reconnect the injured spinal cord conduction of action potentials by graft axons to reconnect the injured spinal cord conduction of action potentials by graft axons to the DCN target. This study demonstrates the the DCN target. This study demonstrates the the DCN target. This study demonstrates the I. Fischer and J. Bonner ability of NPC to form a neuronal relay across I. Fischer and J. Bonner ability of NPC to form a neuronal relay across I. Fischer and J. Bonner ability of NPC to form a neuronal relay across the injured spinal cord and provides the the injured spinal cord and provides the the injured spinal cord and provides the

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 17 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 17 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 17 ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS framework for the restoration of sensory and tools comes the challenge of investigating framework for the restoration of sensory and tools comes the challenge of investigating framework for the restoration of sensory and tools comes the challenge of investigating possibly motor activity. differences amongst these stem cell types with possibly motor activity. differences amongst these stem cell types with possibly motor activity. differences amongst these stem cell types with regard to the methods by which they are regard to the methods by which they are regard to the methods by which they are O-10 Scientific and Clinical Challenges in generated, heterogeneity of the tissues from O-10 Scientific and Clinical Challenges in generated, heterogeneity of the tissues from O-10 Scientific and Clinical Challenges in generated, heterogeneity of the tissues from using Stem Cells for Investigating and which they are derived, differences in their using Stem Cells for Investigating and which they are derived, differences in their using Stem Cells for Investigating and which they are derived, differences in their Treating Amyotrophic Lateral Sclerosis immunogenicity, and potential tumorogenicity. Treating Amyotrophic Lateral Sclerosis immunogenicity, and potential tumorogenicity. Treating Amyotrophic Lateral Sclerosis immunogenicity, and potential tumorogenicity. Furthermore, educating the public about these Furthermore, educating the public about these Furthermore, educating the public about these N.J. Maragakis challenges and limitations as well as their N.J. Maragakis challenges and limitations as well as their N.J. Maragakis challenges and limitations as well as their Johns Hopkins University Department of promise is the responsibility of the scientific Johns Hopkins University Department of promise is the responsibility of the scientific Johns Hopkins University Department of promise is the responsibility of the scientific Neurology, Baltimore, MD community. Neurology, Baltimore, MD community. Neurology, Baltimore, MD community.

Amyotrophic lateral sclerosis (ALS) is the O-11 Neural Stem Cell Therapy for Stroke: Amyotrophic lateral sclerosis (ALS) is the O-11 Neural Stem Cell Therapy for Stroke: Amyotrophic lateral sclerosis (ALS) is the O-11 Neural Stem Cell Therapy for Stroke: most common form of adult motor neuron Underlying Mechanisms and Clinical most common form of adult motor neuron Underlying Mechanisms and Clinical most common form of adult motor neuron Underlying Mechanisms and Clinical disease in which there is progressive Translation disease in which there is progressive Translation disease in which there is progressive Translation degeneration of both the upper motor neurons in degeneration of both the upper motor neurons in degeneration of both the upper motor neurons in the cortex and the lower motor neurons in the G. K. Steinberg the cortex and the lower motor neurons in the G. K. Steinberg the cortex and the lower motor neurons in the G. K. Steinberg brainstem and spinal cord. Because modeling Department of Neurosurgery and brainstem and spinal cord. Because modeling Department of Neurosurgery and brainstem and spinal cord. Because modeling Department of Neurosurgery and ALS has been largely limited to the use of the Stanford Institute for Neuro-Innovation and ALS has been largely limited to the use of the Stanford Institute for Neuro-Innovation and ALS has been largely limited to the use of the Stanford Institute for Neuro-Innovation and mutant SOD1 animal model of familial ALS, a Translational Neurosciences, Stanford mutant SOD1 animal model of familial ALS, a Translational Neurosciences, Stanford mutant SOD1 animal model of familial ALS, a Translational Neurosciences, Stanford significant proportion of ALS biology has gone University, Stanford, CA, USA significant proportion of ALS biology has gone University, Stanford, CA, USA significant proportion of ALS biology has gone University, Stanford, CA, USA largely unstudied. largely unstudied. largely unstudied. “Stem Cells” from a variety of different Stroke is the leading cause of disability “Stem Cells” from a variety of different Stroke is the leading cause of disability “Stem Cells” from a variety of different Stroke is the leading cause of disability sources are excellent tools for investigating and and the #2 cause of death in the Western world. sources are excellent tools for investigating and and the #2 cause of death in the Western world. sources are excellent tools for investigating and and the #2 cause of death in the Western world. potentially treating a variety of neurological Currently, no clinical therapy exists to restore potentially treating a variety of neurological Currently, no clinical therapy exists to restore potentially treating a variety of neurological Currently, no clinical therapy exists to restore disorders. The relatively new discovery for the neurologic function after stroke. Stem cell disorders. The relatively new discovery for the neurologic function after stroke. Stem cell disorders. The relatively new discovery for the neurologic function after stroke. Stem cell creation of induced pluripotent stem cells transplantation holds great promise for creation of induced pluripotent stem cells transplantation holds great promise for creation of induced pluripotent stem cells transplantation holds great promise for (iPSC) has also allowed the generation of facilitating recovery after stroke. This (iPSC) has also allowed the generation of facilitating recovery after stroke. This (iPSC) has also allowed the generation of facilitating recovery after stroke. This pluripotent stem cells from skin fibroblasts. presentation will discuss the mechanisms pluripotent stem cells from skin fibroblasts. presentation will discuss the mechanisms pluripotent stem cells from skin fibroblasts. presentation will discuss the mechanisms This technique is particularly powerful for underlying behavioral recovery after This technique is particularly powerful for underlying behavioral recovery after This technique is particularly powerful for underlying behavioral recovery after several reasons. 1. It allows for the experimental stroke such as replacement of several reasons. 1. It allows for the experimental stroke such as replacement of several reasons. 1. It allows for the experimental stroke such as replacement of development of neural tissues which cannot be neurons, immunomodulation, and secretion of development of neural tissues which cannot be neurons, immunomodulation, and secretion of development of neural tissues which cannot be neurons, immunomodulation, and secretion of readily sampled from living patients. 2. trophic factors that promote endogenous readily sampled from living patients. 2. trophic factors that promote endogenous readily sampled from living patients. 2. trophic factors that promote endogenous Investigators can develop stem cell lines from plasticity including axonal sprouting, dendritic Investigators can develop stem cell lines from plasticity including axonal sprouting, dendritic Investigators can develop stem cell lines from plasticity including axonal sprouting, dendritic patients with sporadic ALS. 3. Stem cell lines branching and neovascularization. Completed patients with sporadic ALS. 3. Stem cell lines branching and neovascularization. Completed patients with sporadic ALS. 3. Stem cell lines branching and neovascularization. Completed can be derived from groups of patients with and ongoing clinical stem cell trials for stroke can be derived from groups of patients with and ongoing clinical stem cell trials for stroke can be derived from groups of patients with and ongoing clinical stem cell trials for stroke common features thus allowing for comparisons will be reviewed. The complex process of common features thus allowing for comparisons will be reviewed. The complex process of common features thus allowing for comparisons will be reviewed. The complex process of of various disease phenotypes. 4. iPSC allow translating the experimental results into a Phase of various disease phenotypes. 4. iPSC allow translating the experimental results into a Phase of various disease phenotypes. 4. iPSC allow translating the experimental results into a Phase for the differentiation into several neural I clinical trial will be described. for the differentiation into several neural I clinical trial will be described. for the differentiation into several neural I clinical trial will be described. subtypes—each of which has a unique role in subtypes—each of which has a unique role in subtypes—each of which has a unique role in disease onset and progression. 5. Cell lines can O-12 Fate And Function Of NG2+ Glial disease onset and progression. 5. Cell lines can O-12 Fate And Function Of NG2+ Glial disease onset and progression. 5. Cell lines can O-12 Fate And Function Of NG2+ Glial be used to study potential pathways possibly Progenitors In Health And Disease be used to study potential pathways possibly Progenitors In Health And Disease be used to study potential pathways possibly Progenitors In Health And Disease involved in ALS pathogenesis. 6. Candidate involved in ALS pathogenesis. 6. Candidate involved in ALS pathogenesis. 6. Candidate drugs can be screened in specific assays using D.E. Bergles drugs can be screened in specific assays using D.E. Bergles drugs can be screened in specific assays using D.E. Bergles iPSC-derived neural subtypes. The Solomon H. Snyder Department of iPSC-derived neural subtypes. The Solomon H. Snyder Department of iPSC-derived neural subtypes. The Solomon H. Snyder Department of However, with the promise and potential Neuroscience, Johns Hopkins School of However, with the promise and potential Neuroscience, Johns Hopkins School of However, with the promise and potential Neuroscience, Johns Hopkins School of that comes with the broad array of stem cells as Medicine, Baltimore, MD that comes with the broad array of stem cells as Medicine, Baltimore, MD that comes with the broad array of stem cells as Medicine, Baltimore, MD

18 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 18 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 18 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS

The mammalian CNS contains an O-13 Inner Ear Sensory Cells From Stem The mammalian CNS contains an O-13 Inner Ear Sensory Cells From Stem The mammalian CNS contains an O-13 Inner Ear Sensory Cells From Stem abundant, widely distributed population of glial Cells abundant, widely distributed population of glial Cells abundant, widely distributed population of glial Cells cells that expresses the chondroitin sulfate cells that expresses the chondroitin sulfate cells that expresses the chondroitin sulfate proteoglycan NG2 (CSPG4) and the alpha S. Heller proteoglycan NG2 (CSPG4) and the alpha S. Heller proteoglycan NG2 (CSPG4) and the alpha S. Heller receptor for PDGF (PDGF R). Although Otolaryngology, Molecular & Cellular receptor for PDGF (PDGF R). Although Otolaryngology, Molecular & Cellular receptor for PDGF (PDGF R). Although Otolaryngology, Molecular & Cellular initially defined as a class of astrocytes, studies Physiology, Stanford University, Stanford, CA initially defined as a class of astrocytes, studies Physiology, Stanford University, Stanford, CA initially defined as a class of astrocytes, studies Physiology, Stanford University, Stanford, CA completed over the past two decades indicate completed over the past two decades indicate completed over the past two decades indicate that these cells represent a third class of Despite elegant biophysical analyses, the that these cells represent a third class of Despite elegant biophysical analyses, the that these cells represent a third class of Despite elegant biophysical analyses, the macroglia, with properties distinct from molecular mechanisms that underlie our senses macroglia, with properties distinct from molecular mechanisms that underlie our senses macroglia, with properties distinct from molecular mechanisms that underlie our senses astrocytes and oligodendrocytes. These NG2+ of hearing and balance are not fully understood. astrocytes and oligodendrocytes. These NG2+ of hearing and balance are not fully understood. astrocytes and oligodendrocytes. These NG2+ of hearing and balance are not fully understood. cells serve as progenitors for oligodendrocytes A major reason for this lack of knowledge is the cells serve as progenitors for oligodendrocytes A major reason for this lack of knowledge is the cells serve as progenitors for oligodendrocytes A major reason for this lack of knowledge is the (OLs) during early development, and are often paucity of material, a few thousand well-hidden (OLs) during early development, and are often paucity of material, a few thousand well-hidden (OLs) during early development, and are often paucity of material, a few thousand well-hidden referred to as oligodendrocyte precursor cells sensory hair cells per inner ear, compared to, for referred to as oligodendrocyte precursor cells sensory hair cells per inner ear, compared to, for referred to as oligodendrocyte precursor cells sensory hair cells per inner ear, compared to, for (OPCs). However, NG2+ cells remain abundant example, the 140-150 million photoreceptor (OPCs). However, NG2+ cells remain abundant example, the 140-150 million photoreceptor (OPCs). However, NG2+ cells remain abundant example, the 140-150 million photoreceptor in the mature CNS after myelinated tracts have cells per retina. Our goal was to devise an in the mature CNS after myelinated tracts have cells per retina. Our goal was to devise an in the mature CNS after myelinated tracts have cells per retina. Our goal was to devise an been established, accounting for approximately efficient in vitro guidance protocol for been established, accounting for approximately efficient in vitro guidance protocol for been established, accounting for approximately efficient in vitro guidance protocol for 5% of all cells, and they retain the ability to generation of functional hair cell-like cells from 5% of all cells, and they retain the ability to generation of functional hair cell-like cells from 5% of all cells, and they retain the ability to generation of functional hair cell-like cells from proliferate throughout life. These cells undergo a renewable source. This was achieved by proliferate throughout life. These cells undergo a renewable source. This was achieved by proliferate throughout life. These cells undergo a renewable source. This was achieved by dramatic morphological changes and increase utilizing, for the most part, known principles of dramatic morphological changes and increase utilizing, for the most part, known principles of dramatic morphological changes and increase utilizing, for the most part, known principles of their proliferation following acute CNS injury early embryonic development and inner ear their proliferation following acute CNS injury early embryonic development and inner ear their proliferation following acute CNS injury early embryonic development and inner ear and in neurodegenerative diseases; nevertheless, induction. Recapitulation of specific signaling and in neurodegenerative diseases; nevertheless, induction. Recapitulation of specific signaling and in neurodegenerative diseases; nevertheless, induction. Recapitulation of specific signaling the contribution of these cells to regeneration events in the culture dish led to otic progenitor the contribution of these cells to regeneration events in the culture dish led to otic progenitor the contribution of these cells to regeneration events in the culture dish led to otic progenitor and tissue repair remains uncertain. Over the cells that were able to differentiate into clusters and tissue repair remains uncertain. Over the cells that were able to differentiate into clusters and tissue repair remains uncertain. Over the cells that were able to differentiate into clusters past several years we have developed new lines of nascent and maturing sensory epithelia, past several years we have developed new lines of nascent and maturing sensory epithelia, past several years we have developed new lines of nascent and maturing sensory epithelia, of transgenic mice that have allowed us to featuring cells with hair and supporting cell of transgenic mice that have allowed us to featuring cells with hair and supporting cell of transgenic mice that have allowed us to featuring cells with hair and supporting cell manipulate gene expression within these characteristics. Cytomorphological assessments manipulate gene expression within these characteristics. Cytomorphological assessments manipulate gene expression within these characteristics. Cytomorphological assessments progenitors, track their fate, monitor their revealed that hair cells generated in an in vitro progenitors, track their fate, monitor their revealed that hair cells generated in an in vitro progenitors, track their fate, monitor their revealed that hair cells generated in an in vitro dynamics on timescales of minutes to months in environment grow typical hair bundles of single dynamics on timescales of minutes to months in environment grow typical hair bundles of single dynamics on timescales of minutes to months in environment grow typical hair bundles of single vivo, and selectively ablate these cells from the kinocilia and stereocilia of graded heights. vivo, and selectively ablate these cells from the kinocilia and stereocilia of graded heights. vivo, and selectively ablate these cells from the kinocilia and stereocilia of graded heights. adult CNS. Genetic fate tracing studies using Bundle-bearing cells responded to mechanical adult CNS. Genetic fate tracing studies using Bundle-bearing cells responded to mechanical adult CNS. Genetic fate tracing studies using Bundle-bearing cells responded to mechanical these mice indicate that NG2+ cells are lineage stimulation with currents that were reminiscent these mice indicate that NG2+ cells are lineage stimulation with currents that were reminiscent these mice indicate that NG2+ cells are lineage stimulation with currents that were reminiscent restricted progenitors that either remain as of transduction currents. Our guidance method restricted progenitors that either remain as of transduction currents. Our guidance method restricted progenitors that either remain as of transduction currents. Our guidance method progenitors or differentiate into offers a platform for molecular studies on hair progenitors or differentiate into offers a platform for molecular studies on hair progenitors or differentiate into offers a platform for molecular studies on hair oligodendrocytes, but do not transdifferentiate cells, which are otherwise difficult to obtain in oligodendrocytes, but do not transdifferentiate cells, which are otherwise difficult to obtain in oligodendrocytes, but do not transdifferentiate cells, which are otherwise difficult to obtain in into astrocytes or neurons, a behavior that is large numbers. Likewise, intermediate into astrocytes or neurons, a behavior that is large numbers. Likewise, intermediate into astrocytes or neurons, a behavior that is large numbers. Likewise, intermediate maintained in neurodegenerative disease presumptively otic cell types, generated by maintained in neurodegenerative disease presumptively otic cell types, generated by maintained in neurodegenerative disease presumptively otic cell types, generated by (amyotrophic lateral sclerosis). In vivo, time applying inner ear developmental principals, are (amyotrophic lateral sclerosis). In vivo, time applying inner ear developmental principals, are (amyotrophic lateral sclerosis). In vivo, time applying inner ear developmental principals, are lapse imaging has revealed that NG2+ cells are emerging as useful in vitro tools to study lapse imaging has revealed that NG2+ cells are emerging as useful in vitro tools to study lapse imaging has revealed that NG2+ cells are emerging as useful in vitro tools to study highly dynamic in the adult mouse cortex. They specific signaling pathways that function during highly dynamic in the adult mouse cortex. They specific signaling pathways that function during highly dynamic in the adult mouse cortex. They specific signaling pathways that function during continually reorient their processes and migrate inner ear development. The fact that in vitro- continually reorient their processes and migrate inner ear development. The fact that in vitro- continually reorient their processes and migrate inner ear development. The fact that in vitro- through tissue to sites of injury to participate in generated hair cell-like cells are functional through tissue to sites of injury to participate in generated hair cell-like cells are functional through tissue to sites of injury to participate in generated hair cell-like cells are functional the formation of glial scars. Together, these shows that generation of replacement hair cells the formation of glial scars. Together, these shows that generation of replacement hair cells the formation of glial scars. Together, these shows that generation of replacement hair cells results suggest that NG2+ glial cells have from pluripotent stem cells is feasible, a finding results suggest that NG2+ glial cells have from pluripotent stem cells is feasible, a finding results suggest that NG2+ glial cells have from pluripotent stem cells is feasible, a finding prominent roles in regeneration and repair in the that justifies the development of stem cell-based prominent roles in regeneration and repair in the that justifies the development of stem cell-based prominent roles in regeneration and repair in the that justifies the development of stem cell-based adult CNS. adult CNS. adult CNS.

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 19 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 19 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 19 ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS treatment strategies for hearing and balance injury is, at least in animal models of the treatment strategies for hearing and balance injury is, at least in animal models of the treatment strategies for hearing and balance injury is, at least in animal models of the disorders. disease, well understood. However, while more disorders. disease, well understood. However, while more disorders. disease, well understood. However, while more than 700 interventions have published efficacy than 700 interventions have published efficacy than 700 interventions have published efficacy O-14 Implications Of Replications: in animal stroke models, around 150 have been O-14 Implications Of Replications: in animal stroke models, around 150 have been O-14 Implications Of Replications: in animal stroke models, around 150 have been Improving The Quality Of Preclinical tested, and been found to be ineffective, in Improving The Quality Of Preclinical tested, and been found to be ineffective, in Improving The Quality Of Preclinical tested, and been found to be ineffective, in Research human stroke studies. If the animal models Research human stroke studies. If the animal models Research human stroke studies. If the animal models faithfully represent human pathophysiology faithfully represent human pathophysiology faithfully represent human pathophysiology N. Kleitman (and what evidence there is suggests that this is, N. Kleitman (and what evidence there is suggests that this is, N. Kleitman (and what evidence there is suggests that this is, National Institute of Neurological for the most part, the case) there are two National Institute of Neurological for the most part, the case) there are two National Institute of Neurological for the most part, the case) there are two Disorders and Stroke, NIH, Bethesda, MD. potential explanations for the systematic failure Disorders and Stroke, NIH, Bethesda, MD. potential explanations for the systematic failure Disorders and Stroke, NIH, Bethesda, MD. potential explanations for the systematic failure of animal experiments to identify effective of animal experiments to identify effective of animal experiments to identify effective The 2009 International Symposium for human neuroprotectants; either the clinical trials The 2009 International Symposium for human neuroprotectants; either the clinical trials The 2009 International Symposium for human neuroprotectants; either the clinical trials Neural Regeneration included a session have been falsely negative, or the animal studies Neural Regeneration included a session have been falsely negative, or the animal studies Neural Regeneration included a session have been falsely negative, or the animal studies presenting the goals and results of the National have been falsely positive. There are a number presenting the goals and results of the National have been falsely positive. There are a number presenting the goals and results of the National have been falsely positive. There are a number Institute of Neurological Disorders and Stroke of potential reasons for the later. In the pre- Institute of Neurological Disorders and Stroke of potential reasons for the later. In the pre- Institute of Neurological Disorders and Stroke of potential reasons for the later. In the pre- (NINDS) Facilities of Research Excellence in clinical development of stroke drugs we have (NINDS) Facilities of Research Excellence in clinical development of stroke drugs we have (NINDS) Facilities of Research Excellence in clinical development of stroke drugs we have Spinal Cord Injury (FORE-SCI) replication usually failed to consider the impact of the risk Spinal Cord Injury (FORE-SCI) replication usually failed to consider the impact of the risk Spinal Cord Injury (FORE-SCI) replication usually failed to consider the impact of the risk contracts. This session invoked lively factors such as age, hypertension and diabetes contracts. This session invoked lively factors such as age, hypertension and diabetes contracts. This session invoked lively factors such as age, hypertension and diabetes discussion and substantial interest in the that define the bulk of the ischemic stroke discussion and substantial interest in the that define the bulk of the ischemic stroke discussion and substantial interest in the that define the bulk of the ischemic stroke importance and inherent difficulties of population. For example, where efficacy has importance and inherent difficulties of population. For example, where efficacy has importance and inherent difficulties of population. For example, where efficacy has reproducing published observations in complex been reported in the context of hypertension, it reproducing published observations in complex been reported in the context of hypertension, it reproducing published observations in complex been reported in the context of hypertension, it preclinical models. A review of the goals and is usually substantially lower. The interpretation preclinical models. A review of the goals and is usually substantially lower. The interpretation preclinical models. A review of the goals and is usually substantially lower. The interpretation the results of continuing NINDS FORE-SCI of animal studies may also have exaggerated the results of continuing NINDS FORE-SCI of animal studies may also have exaggerated the results of continuing NINDS FORE-SCI of animal studies may also have exaggerated studies will be presented, highlighting findings drug efficacy, distorting the selection of drugs studies will be presented, highlighting findings drug efficacy, distorting the selection of drugs studies will be presented, highlighting findings drug efficacy, distorting the selection of drugs from recent replications performed at the for clinical trial and creating unreasonable from recent replications performed at the for clinical trial and creating unreasonable from recent replications performed at the for clinical trial and creating unreasonable University of California, Irvine, and the Ohio expectations of clinical efficacy. Possible University of California, Irvine, and the Ohio expectations of clinical efficacy. Possible University of California, Irvine, and the Ohio expectations of clinical efficacy. Possible State University contract sites. Conclusions reasons for this might include systematic flaws State University contract sites. Conclusions reasons for this might include systematic flaws State University contract sites. Conclusions reasons for this might include systematic flaws drawn from these studies and the experience of in experimental design or conduct which have drawn from these studies and the experience of in experimental design or conduct which have drawn from these studies and the experience of in experimental design or conduct which have performing such replications will be presented the effect of exaggerating efficacy, or a performing such replications will be presented the effect of exaggerating efficacy, or a performing such replications will be presented the effect of exaggerating efficacy, or a (Steward et al., Exp. Neurology, in press). In disproportionate publication of positive studies. (Steward et al., Exp. Neurology, in press). In disproportionate publication of positive studies. (Steward et al., Exp. Neurology, in press). In disproportionate publication of positive studies. addition, other NINDS activities designed to Alternatively, clinical studies may have failed addition, other NINDS activities designed to Alternatively, clinical studies may have failed addition, other NINDS activities designed to Alternatively, clinical studies may have failed improve the quality of NINDS-supported statistically to detect a true biologically improve the quality of NINDS-supported statistically to detect a true biologically improve the quality of NINDS-supported statistically to detect a true biologically preclinical and clinical research through significant therapeutic effect where one exists, preclinical and clinical research through significant therapeutic effect where one exists, preclinical and clinical research through significant therapeutic effect where one exists, rigorous study design and transparent reporting perhaps through testing the wrong drug dose, in rigorous study design and transparent reporting perhaps through testing the wrong drug dose, in rigorous study design and transparent reporting perhaps through testing the wrong drug dose, in (NOT-NS-11-023) will be discussed. the wrong type of patients, or given at the wrong (NOT-NS-11-023) will be discussed. the wrong type of patients, or given at the wrong (NOT-NS-11-023) will be discussed. the wrong type of patients, or given at the wrong time, or recruiting too few patients. time, or recruiting too few patients. time, or recruiting too few patients. O-15 AVOIDING BIAS AT THE BENCH O-15 AVOIDING BIAS AT THE BENCH O-15 AVOIDING BIAS AT THE BENCH O-16 The Challenges of Translation: a O-16 The Challenges of Translation: a O-16 The Challenges of Translation: a D.W. Howells Clinical Perspective D.W. Howells Clinical Perspective D.W. Howells Clinical Perspective Melbourne Brain Centre, Florey Melbourne Brain Centre, Florey Melbourne Brain Centre, Florey Neuroscience Institutes, Austin Health, 245 D.P. Lammertse Neuroscience Institutes, Austin Health, 245 D.P. Lammertse Neuroscience Institutes, Austin Health, 245 D.P. Lammertse Burgundy Street, Heidelberg, Victoria 3084, Craig Hospital, Rocky Mountain Burgundy Street, Heidelberg, Victoria 3084, Craig Hospital, Rocky Mountain Burgundy Street, Heidelberg, Victoria 3084, Craig Hospital, Rocky Mountain AUSTRALIA. Regional Spinal Injury System, 3425 South AUSTRALIA. Regional Spinal Injury System, 3425 South AUSTRALIA. Regional Spinal Injury System, 3425 South Every year around 5 million people are Clarkson Street, Englewood, CO 80113-2811 Every year around 5 million people are Clarkson Street, Englewood, CO 80113-2811 Every year around 5 million people are Clarkson Street, Englewood, CO 80113-2811 affected by stroke, and the cellular and affected by stroke, and the cellular and affected by stroke, and the cellular and molecular pathophysiology of ischaemic brain molecular pathophysiology of ischaemic brain molecular pathophysiology of ischaemic brain

20 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 20 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 20 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS

The field of spinal cord injury (SCI) clinical studies of neurodegenerative disorders The field of spinal cord injury (SCI) clinical studies of neurodegenerative disorders The field of spinal cord injury (SCI) clinical studies of neurodegenerative disorders research is now more than 30 years into the era MSCs have demonstrated efficacy in slowing research is now more than 30 years into the era MSCs have demonstrated efficacy in slowing research is now more than 30 years into the era MSCs have demonstrated efficacy in slowing of clinical trials for interventions intended to disease progression. Proposed regenerative of clinical trials for interventions intended to disease progression. Proposed regenerative of clinical trials for interventions intended to disease progression. Proposed regenerative improve neurological outcome, and yet we still approaches to neurological diseases using MSCs improve neurological outcome, and yet we still approaches to neurological diseases using MSCs improve neurological outcome, and yet we still approaches to neurological diseases using MSCs have not achieved a consensus standard-of-care include cell therapies in which cells are have not achieved a consensus standard-of-care include cell therapies in which cells are have not achieved a consensus standard-of-care include cell therapies in which cells are treatment. Motivated by an interest in improving delivered via intracerebral or intrathecal treatment. Motivated by an interest in improving delivered via intracerebral or intrathecal treatment. Motivated by an interest in improving delivered via intracerebral or intrathecal the conduct of clinical trials in SCI as well as injection. Upon transplantation, MSC in the the conduct of clinical trials in SCI as well as injection. Upon transplantation, MSC in the the conduct of clinical trials in SCI as well as injection. Upon transplantation, MSC in the concerns over the growing availability of brain promote endogenous neuronal growth, concerns over the growing availability of brain promote endogenous neuronal growth, concerns over the growing availability of brain promote endogenous neuronal growth, unproven cellular and other experimental encourage synaptic connection from damaged unproven cellular and other experimental encourage synaptic connection from damaged unproven cellular and other experimental encourage synaptic connection from damaged therapies, the International Campaign for Cure neurons, decrease apoptosis, reduce levels of therapies, the International Campaign for Cure neurons, decrease apoptosis, reduce levels of therapies, the International Campaign for Cure neurons, decrease apoptosis, reduce levels of of spinal cord injury Paralysis (ICCP) and free radicals and regulate inflammation. These of spinal cord injury Paralysis (ICCP) and free radicals and regulate inflammation. These of spinal cord injury Paralysis (ICCP) and free radicals and regulate inflammation. These others have published guidelines for clinical abilities are primarily modulated through others have published guidelines for clinical abilities are primarily modulated through others have published guidelines for clinical abilities are primarily modulated through trial design and conduct (Anderson 2005, paracrine actions. Therapies will capitalize upon trial design and conduct (Anderson 2005, paracrine actions. Therapies will capitalize upon trial design and conduct (Anderson 2005, paracrine actions. Therapies will capitalize upon Fawcett 2007, Steeves 2007, Tuszynski 2007, the innate trophic support from MSC or on Fawcett 2007, Steeves 2007, Tuszynski 2007, the innate trophic support from MSC or on Fawcett 2007, Steeves 2007, Tuszynski 2007, the innate trophic support from MSC or on Lammertse 2007). Others have commented on augmented growth factor support, such as Lammertse 2007). Others have commented on augmented growth factor support, such as Lammertse 2007). Others have commented on augmented growth factor support, such as the pre-clinical evidence basis that would justify delivering brain-derived neurotrophic factor the pre-clinical evidence basis that would justify delivering brain-derived neurotrophic factor the pre-clinical evidence basis that would justify delivering brain-derived neurotrophic factor making the critical translational step to human (BDNF) into the brain to support injured making the critical translational step to human (BDNF) into the brain to support injured making the critical translational step to human (BDNF) into the brain to support injured trials (Steeves 2004, Kwon 2010). As the field neurons, using genetically engineered MSC as trials (Steeves 2004, Kwon 2010). As the field neurons, using genetically engineered MSC as trials (Steeves 2004, Kwon 2010). As the field neurons, using genetically engineered MSC as moves forward, there is a growing need for the delivery vehicles (Joyce et al, 2010). MSC moves forward, there is a growing need for the delivery vehicles (Joyce et al, 2010). MSC moves forward, there is a growing need for the delivery vehicles (Joyce et al, 2010). MSC improving the dialogue between pre-clinical and engineered to secrete BDNF have had improving the dialogue between pre-clinical and engineered to secrete BDNF have had improving the dialogue between pre-clinical and engineered to secrete BDNF have had clinical scientists—ideally, the translational path significant effects on reducing disease clinical scientists—ideally, the translational path significant effects on reducing disease clinical scientists—ideally, the translational path significant effects on reducing disease is a two-way street: both bench-to-bedside and phenotype in transgenic HD mice (Dey et al is a two-way street: both bench-to-bedside and phenotype in transgenic HD mice (Dey et al is a two-way street: both bench-to-bedside and phenotype in transgenic HD mice (Dey et al bedside-to-bench. This presentation will cover 2010). We are using immune deficient mouse bedside-to-bench. This presentation will cover 2010). We are using immune deficient mouse bedside-to-bench. This presentation will cover 2010). We are using immune deficient mouse the clinician’s perspective on the challenges and large animal models to test the biosafety of the clinician’s perspective on the challenges and large animal models to test the biosafety of the clinician’s perspective on the challenges and large animal models to test the biosafety of inherent in the design and conduct of clinical human cell products that are therapeutic inherent in the design and conduct of clinical human cell products that are therapeutic inherent in the design and conduct of clinical human cell products that are therapeutic trials in SCI with commentary on the necessary candidates for clinical trials. Phase 1 clinical trials in SCI with commentary on the necessary candidates for clinical trials. Phase 1 clinical trials in SCI with commentary on the necessary candidates for clinical trials. Phase 1 clinical and sufficient evidence—both efficacy and trials to test the safety of MSC injection into the and sufficient evidence—both efficacy and trials to test the safety of MSC injection into the and sufficient evidence—both efficacy and trials to test the safety of MSC injection into the safety, clinical and pre-clinical—that the central nervous system to treat ALS, traumatic safety, clinical and pre-clinical—that the central nervous system to treat ALS, traumatic safety, clinical and pre-clinical—that the central nervous system to treat ALS, traumatic Principal Investigator must consider when brain injury and stroke in humans are currently Principal Investigator must consider when brain injury and stroke in humans are currently Principal Investigator must consider when brain injury and stroke in humans are currently embarking on human subject research. ongoing. The progress toward applying MSC- embarking on human subject research. ongoing. The progress toward applying MSC- embarking on human subject research. ongoing. The progress toward applying MSC- based cellular therapies to the treatment of based cellular therapies to the treatment of based cellular therapies to the treatment of O-17 Working toward cellular therapies to Huntington’s disease will be discussed. O-17 Working toward cellular therapies to Huntington’s disease will be discussed. O-17 Working toward cellular therapies to Huntington’s disease will be discussed. treat Huntington's disease treat Huntington's disease treat Huntington's disease O-18 Matrix Metalloproteinases As O-18 Matrix Metalloproteinases As O-18 Matrix Metalloproteinases As J. A. Nolta Modifiers Of Injury And Recovery Processes J. A. Nolta Modifiers Of Injury And Recovery Processes J. A. Nolta Modifiers Of Injury And Recovery Processes Director, Stem Cell Program, University After Spinal Cord Injury Director, Stem Cell Program, University After Spinal Cord Injury Director, Stem Cell Program, University After Spinal Cord Injury of California Davis, Sacramento CA of California Davis, Sacramento CA of California Davis, Sacramento CA L.J. Noble-Haeusslein L.J. Noble-Haeusslein L.J. Noble-Haeusslein There is much interest in the use of Departments of Neurosurgery and There is much interest in the use of Departments of Neurosurgery and There is much interest in the use of Departments of Neurosurgery and Mesenchymal Stem Cells/Marrow Stromal Cells Physical Therapy and Rehabilitation Science, Mesenchymal Stem Cells/Marrow Stromal Cells Physical Therapy and Rehabilitation Science, Mesenchymal Stem Cells/Marrow Stromal Cells Physical Therapy and Rehabilitation Science, (MSCs) to treat neurodegenerative disorders, University of California, San Francisco, (MSCs) to treat neurodegenerative disorders, University of California, San Francisco, (MSCs) to treat neurodegenerative disorders, University of California, San Francisco, such as Huntington’s disease (HD) and California 94143 USA such as Huntington’s disease (HD) and California 94143 USA such as Huntington’s disease (HD) and California 94143 USA Amyotrophic lateral sclerosis (ALS). MSCs Of over 25 members of the matrix Amyotrophic lateral sclerosis (ALS). MSCs Of over 25 members of the matrix Amyotrophic lateral sclerosis (ALS). MSCs Of over 25 members of the matrix present a promising tool for cell therapy, and are metalloproteinase (MMP) family, MMP-9 is one present a promising tool for cell therapy, and are metalloproteinase (MMP) family, MMP-9 is one present a promising tool for cell therapy, and are metalloproteinase (MMP) family, MMP-9 is one currently being tested in FDA-approved Phase I of the most studied in central nervous system currently being tested in FDA-approved Phase I of the most studied in central nervous system currently being tested in FDA-approved Phase I of the most studied in central nervous system to III clinical trials for many disorders. In pre- injury. Nevertheless, we have yet to fully to III clinical trials for many disorders. In pre- injury. Nevertheless, we have yet to fully to III clinical trials for many disorders. In pre- injury. Nevertheless, we have yet to fully

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 21 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 21 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 21 ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS appreciate its contributions to injury, wound O-19 The Sour Side of Sugars: Chondroitin appreciate its contributions to injury, wound O-19 The Sour Side of Sugars: Chondroitin appreciate its contributions to injury, wound O-19 The Sour Side of Sugars: Chondroitin healing events, and recovery. This is due to the Sulfate Signaling in Axonal Guidance healing events, and recovery. This is due to the Sulfate Signaling in Axonal Guidance healing events, and recovery. This is due to the Sulfate Signaling in Axonal Guidance complex functions of this protease that are complex functions of this protease that are complex functions of this protease that are context/time dependent, its expression in diverse H.M. Geller, J.-H. Yi, P. Yu, H. Wang, Y. context/time dependent, its expression in diverse H.M. Geller, J.-H. Yi, P. Yu, H. Wang, Y. context/time dependent, its expression in diverse H.M. Geller, J.-H. Yi, P. Yu, H. Wang, Y. cell populations, and an ability to engage other Katagiri cell populations, and an ability to engage other Katagiri cell populations, and an ability to engage other Katagiri factors, having opposing or synergistic Developmental Neuroscience Section, factors, having opposing or synergistic Developmental Neuroscience Section, factors, having opposing or synergistic Developmental Neuroscience Section, functions. This is exemplified in studies of National Institutes of Health/National Heart functions. This is exemplified in studies of National Institutes of Health/National Heart functions. This is exemplified in studies of National Institutes of Health/National Heart MMP-9 in the context of barrier dysfunction, Lung Blood Institute, Bethesda, MD MMP-9 in the context of barrier dysfunction, Lung Blood Institute, Bethesda, MD MMP-9 in the context of barrier dysfunction, Lung Blood Institute, Bethesda, MD glial scar formation and leukocyte trafficking in glial scar formation and leukocyte trafficking in glial scar formation and leukocyte trafficking in the injured spinal cord. MMP-9 is expressed Chondroitin sulfate proteoglycans are the injured spinal cord. MMP-9 is expressed Chondroitin sulfate proteoglycans are the injured spinal cord. MMP-9 is expressed Chondroitin sulfate proteoglycans are over the first week post injury with maximal recognized as molecules which repel growing over the first week post injury with maximal recognized as molecules which repel growing over the first week post injury with maximal recognized as molecules which repel growing expression within the first 24 hours after injury. axons. Much of this repellant activity is expression within the first 24 hours after injury. axons. Much of this repellant activity is expression within the first 24 hours after injury. axons. Much of this repellant activity is It is localized to blood vessels in the acutely abolished by treatment with the enzyme It is localized to blood vessels in the acutely abolished by treatment with the enzyme It is localized to blood vessels in the acutely abolished by treatment with the enzyme injured cord and contributes to early disruption chondroitinase ABC, which digests the injured cord and contributes to early disruption chondroitinase ABC, which digests the injured cord and contributes to early disruption chondroitinase ABC, which digests the of the barrier. In the chronically injured cord, chondroitin sulfate glycosaminoglyan (GAG) of the barrier. In the chronically injured cord, chondroitin sulfate glycosaminoglyan (GAG) of the barrier. In the chronically injured cord, chondroitin sulfate glycosaminoglyan (GAG) MMP-9 is up regulated in astrocytes. Formation chains, leaving the proteins intact. MMP-9 is up regulated in astrocytes. Formation chains, leaving the proteins intact. MMP-9 is up regulated in astrocytes. Formation chains, leaving the proteins intact. of an inhibitory glial scar is more prominent in These data support a primary role for CS GAG of an inhibitory glial scar is more prominent in These data support a primary role for CS GAG of an inhibitory glial scar is more prominent in These data support a primary role for CS GAG spinal cord injured MMP-9 null mice relative to chains as active signaling molecules. CS GAG spinal cord injured MMP-9 null mice relative to chains as active signaling molecules. CS GAG spinal cord injured MMP-9 null mice relative to chains as active signaling molecules. CS GAG wild-type controls. In vitro studies confirm the chains are heterogeneous, comprised of a series wild-type controls. In vitro studies confirm the chains are heterogeneous, comprised of a series wild-type controls. In vitro studies confirm the chains are heterogeneous, comprised of a series specificity of MMP-9 directed migration of of sulfated disaccharides of glucuronic acid specificity of MMP-9 directed migration of of sulfated disaccharides of glucuronic acid specificity of MMP-9 directed migration of of sulfated disaccharides of glucuronic acid astrocytes. Finally, MMP-9 is integral to (GlcA) and N-acetyl-galactosamine (GalNAc), astrocytes. Finally, MMP-9 is integral to (GlcA) and N-acetyl-galactosamine (GalNAc), astrocytes. Finally, MMP-9 is integral to (GlcA) and N-acetyl-galactosamine (GalNAc), leukocyte recruitment and trafficking. This varying both in the length of the GAG chain and leukocyte recruitment and trafficking. This varying both in the length of the GAG chain and leukocyte recruitment and trafficking. This varying both in the length of the GAG chain and protease is utilized by neutrophils to the disaccharide composition. Our data support protease is utilized by neutrophils to the disaccharide composition. Our data support protease is utilized by neutrophils to the disaccharide composition. Our data support transmigrate into the injured cord. Moreover, 4-sulfation GalNAc of as being responsible for transmigrate into the injured cord. Moreover, 4-sulfation GalNAc of as being responsible for transmigrate into the injured cord. Moreover, 4-sulfation GalNAc of as being responsible for neutrophils constitute the primary source of the signaling by CS GAG chains to neutrophils constitute the primary source of the signaling by CS GAG chains to neutrophils constitute the primary source of the signaling by CS GAG chains to MMP-9 in the acutely injured cord. Recent neurons. We will discuss biochemical data and MMP-9 in the acutely injured cord. Recent neurons. We will discuss biochemical data and MMP-9 in the acutely injured cord. Recent neurons. We will discuss biochemical data and studies reveal a synergistic partnership between immunocytochemical data on the composition studies reveal a synergistic partnership between immunocytochemical data on the composition studies reveal a synergistic partnership between immunocytochemical data on the composition MMP-9 and SDF-1 in facilitating transmigration and localization of CS GAG chains from normal MMP-9 and SDF-1 in facilitating transmigration and localization of CS GAG chains from normal MMP-9 and SDF-1 in facilitating transmigration and localization of CS GAG chains from normal of monocytes into the injured spinal cord. That and injured brain, as well as functional data of monocytes into the injured spinal cord. That and injured brain, as well as functional data of monocytes into the injured spinal cord. That and injured brain, as well as functional data MMP-9 facilitates the trafficking of both demonstrating the biological activities of CS MMP-9 facilitates the trafficking of both demonstrating the biological activities of CS MMP-9 facilitates the trafficking of both demonstrating the biological activities of CS neutrophils and monocytes is of considerable GAG chains in vitro and anatomical data on the neutrophils and monocytes is of considerable GAG chains in vitro and anatomical data on the neutrophils and monocytes is of considerable GAG chains in vitro and anatomical data on the interest, as we have found that combinatorial binding of CS GAG chains to brain. We will interest, as we have found that combinatorial binding of CS GAG chains to brain. We will interest, as we have found that combinatorial binding of CS GAG chains to brain. We will strategies to reduce the infiltration of these also address the signal transduction pathways strategies to reduce the infiltration of these also address the signal transduction pathways strategies to reduce the infiltration of these also address the signal transduction pathways leukocytes, enhances neurologic recovery. In used downstream of putative receptors for CS leukocytes, enhances neurologic recovery. In used downstream of putative receptors for CS leukocytes, enhances neurologic recovery. In used downstream of putative receptors for CS summary, improved neurologic recovery in GAG chains. summary, improved neurologic recovery in GAG chains. summary, improved neurologic recovery in GAG chains. spinal cord injured MMP-9 null animals may be spinal cord injured MMP-9 null animals may be spinal cord injured MMP-9 null animals may be attributed to diverse, adverse roles for MMP-9, O-20 Identification and Functional attributed to diverse, adverse roles for MMP-9, O-20 Identification and Functional attributed to diverse, adverse roles for MMP-9, O-20 Identification and Functional propagated by different cells types that Characterization of Novel Receptors for propagated by different cells types that Characterization of Novel Receptors for propagated by different cells types that Characterization of Novel Receptors for contribute to the early injury response and direct Inhibitory Chondroitin Sulfate Proteoglycans contribute to the early injury response and direct Inhibitory Chondroitin Sulfate Proteoglycans contribute to the early injury response and direct Inhibitory Chondroitin Sulfate Proteoglycans aberrant wound healing. aberrant wound healing. aberrant wound healing. Supported by NIH (RO1NS039278), the DANA R.J. Giger Supported by NIH (RO1NS039278), the DANA R.J. Giger Supported by NIH (RO1NS039278), the DANA R.J. Giger Foundation, Oxnard Foundation, Roman Reed University of Michigan School of Foundation, Oxnard Foundation, Roman Reed University of Michigan School of Foundation, Oxnard Foundation, Roman Reed University of Michigan School of Fund from the State of California, and Craig H. Medicine, Department of Cell & Developmental Fund from the State of California, and Craig H. Medicine, Department of Cell & Developmental Fund from the State of California, and Craig H. Medicine, Department of Cell & Developmental Neilson Foundation Biology and Department of Neurology, Ann Neilson Foundation Biology and Department of Neurology, Ann Neilson Foundation Biology and Department of Neurology, Ann Arbor, Michigan 48109-2200. Arbor, Michigan 48109-2200. Arbor, Michigan 48109-2200.

22 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 22 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 22 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS

Following injury to the adult mammalian controls. A similar release of inhibition was Following injury to the adult mammalian controls. A similar release of inhibition was Following injury to the adult mammalian controls. A similar release of inhibition was CNS, severed axons do not regenerate beyond obtained with CGNs obtained from mice null CNS, severed axons do not regenerate beyond obtained with CGNs obtained from mice null CNS, severed axons do not regenerate beyond obtained with CGNs obtained from mice null the lesion site, often leading to permanent for RPTPσ, a previously identified CSPG the lesion site, often leading to permanent for RPTPσ, a previously identified CSPG the lesion site, often leading to permanent for RPTPσ, a previously identified CSPG functional deficits. Multiple lines of evidence receptor. NgR1,2,3-/- triple null mice are viable functional deficits. Multiple lines of evidence receptor. NgR1,2,3-/- triple null mice are viable functional deficits. Multiple lines of evidence receptor. NgR1,2,3-/- triple null mice are viable suggest that growth inhibitory molecules in into adulthood and show no obvious neurologic suggest that growth inhibitory molecules in into adulthood and show no obvious neurologic suggest that growth inhibitory molecules in into adulthood and show no obvious neurologic CNS myelin (including Nogo, MAG, OMgp) phenotype. To examine whether loss of all three CNS myelin (including Nogo, MAG, OMgp) phenotype. To examine whether loss of all three CNS myelin (including Nogo, MAG, OMgp) phenotype. To examine whether loss of all three and chondroitin sulfate proteoglycans (CSPGs) NgRs leads to enhanced regeneration of severed and chondroitin sulfate proteoglycans (CSPGs) NgRs leads to enhanced regeneration of severed and chondroitin sulfate proteoglycans (CSPGs) NgRs leads to enhanced regeneration of severed associated with glial scar tissue contribute to the retinal ganglion cell axons, adult mice were associated with glial scar tissue contribute to the retinal ganglion cell axons, adult mice were associated with glial scar tissue contribute to the retinal ganglion cell axons, adult mice were growth inhibitory nature of the injured adult subjected to optic nerve injury. The combined growth inhibitory nature of the injured adult subjected to optic nerve injury. The combined growth inhibitory nature of the injured adult subjected to optic nerve injury. The combined mammalian CNS tissue. CSPGs are a diverse loss of NgR1, NgR2, and NgR3 leads to mammalian CNS tissue. CSPGs are a diverse loss of NgR1, NgR2, and NgR3 leads to mammalian CNS tissue. CSPGs are a diverse loss of NgR1, NgR2, and NgR3 leads to family of extracellular matrix glycoproteins, enhanced axonal regeneration following retro- family of extracellular matrix glycoproteins, enhanced axonal regeneration following retro- family of extracellular matrix glycoproteins, enhanced axonal regeneration following retro- members of which have been shown to function orbital optic nerve injury as assessed by anti- members of which have been shown to function orbital optic nerve injury as assessed by anti- members of which have been shown to function orbital optic nerve injury as assessed by anti- as potent inhibitors of neurite outgrowth in GAP43 immunolabeling. The combined loss of as potent inhibitors of neurite outgrowth in GAP43 immunolabeling. The combined loss of as potent inhibitors of neurite outgrowth in GAP43 immunolabeling. The combined loss of vitro. Enzymatic digestion of CSPG the MAI receptors NgR1 and NgR2, however, is vitro. Enzymatic digestion of CSPG the MAI receptors NgR1 and NgR2, however, is vitro. Enzymatic digestion of CSPG the MAI receptors NgR1 and NgR2, however, is glycosaminoglycan (GAG) chains with not sufficient to promote axonal regeneration. glycosaminoglycan (GAG) chains with not sufficient to promote axonal regeneration. glycosaminoglycan (GAG) chains with not sufficient to promote axonal regeneration. chondroitinase ABC lyase (ChaseABC) Collectively, these results identify NgR1 and chondroitinase ABC lyase (ChaseABC) Collectively, these results identify NgR1 and chondroitinase ABC lyase (ChaseABC) Collectively, these results identify NgR1 and promotes experience-dependent neuronal NgR3 as novel CSPG receptors, demonstrate promotes experience-dependent neuronal NgR3 as novel CSPG receptors, demonstrate promotes experience-dependent neuronal NgR3 as novel CSPG receptors, demonstrate plasticity in the adult visual cortex and leads to functional redundancy among Nogo receptors, plasticity in the adult visual cortex and leads to functional redundancy among Nogo receptors, plasticity in the adult visual cortex and leads to functional redundancy among Nogo receptors, improved behavioral outcomes following spinal and provide unexpected evidence for shared improved behavioral outcomes following spinal and provide unexpected evidence for shared improved behavioral outcomes following spinal and provide unexpected evidence for shared cord injury in vivo. mechanisms of MAI and CSPG inhibition. cord injury in vivo. mechanisms of MAI and CSPG inhibition. cord injury in vivo. mechanisms of MAI and CSPG inhibition. Here we report on a novel interaction Here we report on a novel interaction Here we report on a novel interaction between select members of the Nogo receptor O-21 Oligodendrocyte Support Of Axon between select members of the Nogo receptor O-21 Oligodendrocyte Support Of Axon between select members of the Nogo receptor O-21 Oligodendrocyte Support Of Axon family (NgRs) and CSPGs. NgR1 and NgR3, Function And Integrity family (NgRs) and CSPGs. NgR1 and NgR3, Function And Integrity family (NgRs) and CSPGs. NgR1 and NgR3, Function And Integrity but not NgR2, bind strongly to the but not NgR2, bind strongly to the but not NgR2, bind strongly to the glycosaminoglycan (GAG) chain of neural K.-A. Nave*, U. Fuenschilling, L. Supplie, F. glycosaminoglycan (GAG) chain of neural K.-A. Nave*, U. Fuenschilling, L. Supplie, F. glycosaminoglycan (GAG) chain of neural K.-A. Nave*, U. Fuenschilling, L. Supplie, F. CSPGs. Soluble NgR1 and NgR3 bind in a Kirchhoff, A. Saab, I. Tzvetanova, C. Moraes, CSPGs. Soluble NgR1 and NgR3 bind in a Kirchhoff, A. Saab, I. Tzvetanova, C. Moraes, CSPGs. Soluble NgR1 and NgR3 bind in a Kirchhoff, A. Saab, I. Tzvetanova, C. Moraes, ChaseABC-sensitive manner to postnatal-day D. Mahad, J. Edgar, S. Beltan, J. Frahm., S. ChaseABC-sensitive manner to postnatal-day D. Mahad, J. Edgar, S. Beltan, J. Frahm., S. ChaseABC-sensitive manner to postnatal-day D. Mahad, J. Edgar, S. Beltan, J. Frahm., S. (P)1 rat brain tissue sections. Soluble NgR1 and Boretius (P)1 rat brain tissue sections. Soluble NgR1 and Boretius (P)1 rat brain tissue sections. Soluble NgR1 and Boretius NgR3 bind strongly to optic nerve tissue *Max Planck Institute of Experimental NgR3 bind strongly to optic nerve tissue *Max Planck Institute of Experimental NgR3 bind strongly to optic nerve tissue *Max Planck Institute of Experimental sections of adult mice subjected to retro-orbital Medicine, Department of Neurogenetics, D- sections of adult mice subjected to retro-orbital Medicine, Department of Neurogenetics, D- sections of adult mice subjected to retro-orbital Medicine, Department of Neurogenetics, D- crush injury to the optic nerve. A much weaker 37075 Göttingen, Germany crush injury to the optic nerve. A much weaker 37075 Göttingen, Germany crush injury to the optic nerve. A much weaker 37075 Göttingen, Germany binding of soluble receptors is observed to binding of soluble receptors is observed to binding of soluble receptors is observed to control (uninjured) optic nerve tissue. We have Oligodendrocytes maintain axon function and control (uninjured) optic nerve tissue. We have Oligodendrocytes maintain axon function and control (uninjured) optic nerve tissue. We have Oligodendrocytes maintain axon function and mapped the CS-GAG binding motif on NgR1 survival in myelinated fiber tracts. Specifically, mapped the CS-GAG binding motif on NgR1 survival in myelinated fiber tracts. Specifically, mapped the CS-GAG binding motif on NgR1 survival in myelinated fiber tracts. Specifically, and show that it is distinct from the binding site we have hypothesized that myelinating glia and show that it is distinct from the binding site we have hypothesized that myelinating glia and show that it is distinct from the binding site we have hypothesized that myelinating glia of Nogo, MAG, and OMgp. A soluble form of provide trophic support, however the underlying of Nogo, MAG, and OMgp. A soluble form of provide trophic support, however the underlying of Nogo, MAG, and OMgp. A soluble form of provide trophic support, however the underlying the NgR1 GAG binding motif promotes neurite mechanisms are not understood. Recently, we the NgR1 GAG binding motif promotes neurite mechanisms are not understood. Recently, we the NgR1 GAG binding motif promotes neurite mechanisms are not understood. Recently, we outgrowth of cerebellar neurons plated on a obtained evidence for a metabolic component of outgrowth of cerebellar neurons plated on a obtained evidence for a metabolic component of outgrowth of cerebellar neurons plated on a obtained evidence for a metabolic component of mixture of substrate adsorbed CSPGs. neuron-glia interactions by targeting a null mixture of substrate adsorbed CSPGs. neuron-glia interactions by targeting a null mixture of substrate adsorbed CSPGs. neuron-glia interactions by targeting a null Loss-of-function experiments revealed that mutation of the Cox10 (protoheme IX Loss-of-function experiments revealed that mutation of the Cox10 (protoheme IX Loss-of-function experiments revealed that mutation of the Cox10 (protoheme IX NgRs are important for CSPG mediated farnesyltransferase) gene to myelinating glial NgRs are important for CSPG mediated farnesyltransferase) gene to myelinating glial NgRs are important for CSPG mediated farnesyltransferase) gene to myelinating glial inhibition of neurite outgrowth. Primary cells. This gene encodes the hemeA-farnesyl inhibition of neurite outgrowth. Primary cells. This gene encodes the hemeA-farnesyl inhibition of neurite outgrowth. Primary cells. This gene encodes the hemeA-farnesyl cerebellar granule neurons (CGNs) isolated transferase, essential for the assembly of the cerebellar granule neurons (CGNs) isolated transferase, essential for the assembly of the cerebellar granule neurons (CGNs) isolated transferase, essential for the assembly of the from NgR1, NgR2, NgR3 triple mutant cytochrome c oxidase (COX) complex IV in from NgR1, NgR2, NgR3 triple mutant cytochrome c oxidase (COX) complex IV in from NgR1, NgR2, NgR3 triple mutant cytochrome c oxidase (COX) complex IV in (NgR1,2,3-/-) mice grow longer neurites on mitochondria. In the absence of COX10, newly (NgR1,2,3-/-) mice grow longer neurites on mitochondria. In the absence of COX10, newly (NgR1,2,3-/-) mice grow longer neurites on mitochondria. In the absence of COX10, newly CSPGs than CGNs isolated from wild-type synthesized complex IV is unstable and rapidly CSPGs than CGNs isolated from wild-type synthesized complex IV is unstable and rapidly CSPGs than CGNs isolated from wild-type synthesized complex IV is unstable and rapidly

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 23 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 23 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 23 ORAL PRESENTATIONS ORAL PRESENTATIONS ORAL PRESENTATIONS degraded. In the peripheral nervous system, functions, and to assess the roles that specific degraded. In the peripheral nervous system, functions, and to assess the roles that specific degraded. In the peripheral nervous system, functions, and to assess the roles that specific these mutants exhibit a novel neuropathy sets of neurons play within neural circuits, it these mutants exhibit a novel neuropathy sets of neurons play within neural circuits, it these mutants exhibit a novel neuropathy sets of neurons play within neural circuits, it phenotype with dysmyelination, axonal would ideally be possible to drive or quiet the phenotype with dysmyelination, axonal would ideally be possible to drive or quiet the phenotype with dysmyelination, axonal would ideally be possible to drive or quiet the degeneration, muscle atrophy, and paralysis. activity of defined neurons embedded within an degeneration, muscle atrophy, and paralysis. activity of defined neurons embedded within an degeneration, muscle atrophy, and paralysis. activity of defined neurons embedded within an Surprisingly in the CNS, depletion of intact neural network. Over the last few years, Surprisingly in the CNS, depletion of intact neural network. Over the last few years, Surprisingly in the CNS, depletion of intact neural network. Over the last few years, mitochondrial respiratory functions from mature we have developed a number of genetically- mitochondrial respiratory functions from mature we have developed a number of genetically- mitochondrial respiratory functions from mature we have developed a number of genetically- oligodendrocytes did not cause demyelination, encoded tools that enable the electrical activity oligodendrocytes did not cause demyelination, encoded tools that enable the electrical activity oligodendrocytes did not cause demyelination, encoded tools that enable the electrical activity axonal degeneration, or secondary inflammation of neurons to be activated or silenced by pulses axonal degeneration, or secondary inflammation of neurons to be activated or silenced by pulses axonal degeneration, or secondary inflammation of neurons to be activated or silenced by pulses in the CNS. In contrast to cultured of light. These molecules are microbial opsins, in the CNS. In contrast to cultured of light. These molecules are microbial opsins, in the CNS. In contrast to cultured of light. These molecules are microbial opsins, oligodendrocytes, which die upon inactivation seven-transmembrane proteins adapted from oligodendrocytes, which die upon inactivation seven-transmembrane proteins adapted from oligodendrocytes, which die upon inactivation seven-transmembrane proteins adapted from of complex IV, post-myelination organisms found throughout the world, which of complex IV, post-myelination organisms found throughout the world, which of complex IV, post-myelination organisms found throughout the world, which oligodendrocytes survive in vivo by aerobic react to light by transporting ions across the oligodendrocytes survive in vivo by aerobic react to light by transporting ions across the oligodendrocytes survive in vivo by aerobic react to light by transporting ions across the glycolysis. Using magnetic resonance lipid membranes of cells in which they are glycolysis. Using magnetic resonance lipid membranes of cells in which they are glycolysis. Using magnetic resonance lipid membranes of cells in which they are spectroscopy, we found brain lactate levels genetically expressed. Beginning with the light- spectroscopy, we found brain lactate levels genetically expressed. Beginning with the light- spectroscopy, we found brain lactate levels genetically expressed. Beginning with the light- increased, but only in mice exposed to volatile gated inward cation channel channelrhodopsin- increased, but only in mice exposed to volatile gated inward cation channel channelrhodopsin- increased, but only in mice exposed to volatile gated inward cation channel channelrhodopsin- anaesthetics that inhibit respiration. This 2, adapted from the green alga C. reinhardtii anaesthetics that inhibit respiration. This 2, adapted from the green alga C. reinhardtii anaesthetics that inhibit respiration. This 2, adapted from the green alga C. reinhardtii demonstrates that glycolysis products can be and the light-driven inward chloride pump demonstrates that glycolysis products can be and the light-driven inward chloride pump demonstrates that glycolysis products can be and the light-driven inward chloride pump efficiently shuttled out of oligodendrocytes and halorhodopsin, adapted from the archaeon N. efficiently shuttled out of oligodendrocytes and halorhodopsin, adapted from the archaeon N. efficiently shuttled out of oligodendrocytes and halorhodopsin, adapted from the archaeon N. utilized in the normal appearing white matter. In pharaonis, we have mined genomic resources utilized in the normal appearing white matter. In pharaonis, we have mined genomic resources utilized in the normal appearing white matter. In pharaonis, we have mined genomic resources conditional mouse mutants lacking NMDA from across the tree of life to discover reagents conditional mouse mutants lacking NMDA from across the tree of life to discover reagents conditional mouse mutants lacking NMDA from across the tree of life to discover reagents receptors from oligodendrocytes, we find that that support high-performance, multiple-color, receptors from oligodendrocytes, we find that that support high-performance, multiple-color, receptors from oligodendrocytes, we find that that support high-performance, multiple-color, glial support of axonal energy metabolisms is control of the electrical activity of defined glial support of axonal energy metabolisms is control of the electrical activity of defined glial support of axonal energy metabolisms is control of the electrical activity of defined significantly compromised. We suggest that neural substrates in the brain. Recently for significantly compromised. We suggest that neural substrates in the brain. Recently for significantly compromised. We suggest that neural substrates in the brain. Recently for oligodendroglial-axonal metabolic coupling is example we demonstrated that molecules from oligodendroglial-axonal metabolic coupling is example we demonstrated that molecules from oligodendroglial-axonal metabolic coupling is example we demonstrated that molecules from likely to serve a physiological function in different kingdoms of life enable powerful, likely to serve a physiological function in different kingdoms of life enable powerful, likely to serve a physiological function in different kingdoms of life enable powerful, myelinated tracts, and that its perturbation multi-color silencing of different sets of myelinated tracts, and that its perturbation multi-color silencing of different sets of myelinated tracts, and that its perturbation multi-color silencing of different sets of contributes to axonal degeneration (Supported neurons. We have also discovered molecules contributes to axonal degeneration (Supported neurons. We have also discovered molecules contributes to axonal degeneration (Supported neurons. We have also discovered molecules by an ERC Advanced Investigator Grant). that enable 100% shutdown of neural activity in by an ERC Advanced Investigator Grant). that enable 100% shutdown of neural activity in by an ERC Advanced Investigator Grant). that enable 100% shutdown of neural activity in awake behaving mice and non-human primates, awake behaving mice and non-human primates, awake behaving mice and non-human primates, O-22 Optogenetics: Tools For Controlling in response to light. We have also developed O-22 Optogenetics: Tools For Controlling in response to light. We have also developed O-22 Optogenetics: Tools For Controlling in response to light. We have also developed Brain Circuits With Light microfabricated light sources capable of Brain Circuits With Light microfabricated light sources capable of Brain Circuits With Light microfabricated light sources capable of delivering light into complexly-shaped, 3-D, delivering light into complexly-shaped, 3-D, delivering light into complexly-shaped, 3-D, E. S. Boyden distributed neural circuits. These tools are E. S. Boyden distributed neural circuits. These tools are E. S. Boyden distributed neural circuits. These tools are MIT Media Lab and McGovern Institute, enabling the causal assessment of the roles that MIT Media Lab and McGovern Institute, enabling the causal assessment of the roles that MIT Media Lab and McGovern Institute, enabling the causal assessment of the roles that Depts. of Biological Engineering and Brain and different sets of neurons play within neural Depts. of Biological Engineering and Brain and different sets of neurons play within neural Depts. of Biological Engineering and Brain and different sets of neurons play within neural Cognitive Sciences, Massachusetts Institute of circuits, and are accordingly being used by Cognitive Sciences, Massachusetts Institute of circuits, and are accordingly being used by Cognitive Sciences, Massachusetts Institute of circuits, and are accordingly being used by Technology, Cambridge, MA hundreds of groups to reveal how different sets Technology, Cambridge, MA hundreds of groups to reveal how different sets Technology, Cambridge, MA hundreds of groups to reveal how different sets of neurons contribute to the emergent of neurons contribute to the emergent of neurons contribute to the emergent Understanding how different kinds of computational and behavioral functions of the Understanding how different kinds of computational and behavioral functions of the Understanding how different kinds of computational and behavioral functions of the neuron in the brain work together to implement brain. These tools are also being explored as neuron in the brain work together to implement brain. These tools are also being explored as neuron in the brain work together to implement brain. These tools are also being explored as sensations, feelings, thoughts, and movements, components of prototype neural control sensations, feelings, thoughts, and movements, components of prototype neural control sensations, feelings, thoughts, and movements, components of prototype neural control and how deficits in specific kinds of neuron prosthetics capable of correcting neural circuit and how deficits in specific kinds of neuron prosthetics capable of correcting neural circuit and how deficits in specific kinds of neuron prosthetics capable of correcting neural circuit result in brain diseases, has long been a priority computations that have gone awry in brain result in brain diseases, has long been a priority computations that have gone awry in brain result in brain diseases, has long been a priority computations that have gone awry in brain in basic and clinical neuroscience. In order to disorders, and we recently have begun to in basic and clinical neuroscience. In order to disorders, and we recently have begun to in basic and clinical neuroscience. In order to disorders, and we recently have begun to determine how different kinds of neurons in the conduct pre-clinical tests of the safety and determine how different kinds of neurons in the conduct pre-clinical tests of the safety and determine how different kinds of neurons in the conduct pre-clinical tests of the safety and brain work together to implement brain efficacy of these molecules in non-human brain work together to implement brain efficacy of these molecules in non-human brain work together to implement brain efficacy of these molecules in non-human primates. primates. primates.

24 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 24 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 24 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

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SESSION ONE SESSION ONE SESSION ONE

P-1 Impaired Degeneration And Regeneration Of Peripheral Motor Axons Of Mice P-1 Impaired Degeneration And Regeneration Of Peripheral Motor Axons Of Mice P-1 Impaired Degeneration And Regeneration Of Peripheral Motor Axons Of Mice Heterozygously Deficient For The Myelin Protein P0 Gene Heterozygously Deficient For The Myelin Protein P0 Gene Heterozygously Deficient For The Myelin Protein P0 Gene M. Moldovan, M. Rosberg, J. Vikeså, F. C. Nielsen, C. Krarup M. Moldovan, M. Rosberg, J. Vikeså, F. C. Nielsen, C. Krarup M. Moldovan, M. Rosberg, J. Vikeså, F. C. Nielsen, C. Krarup

P-2 Does The Canonical Wound Healing Model Help To Explain The Pathogenesis P-2 Does The Canonical Wound Healing Model Help To Explain The Pathogenesis P-2 Does The Canonical Wound Healing Model Help To Explain The Pathogenesis Of Compression Neuropathies? Of Compression Neuropathies? Of Compression Neuropathies? M. Lin; P. Hahn; J. Kang; D. Frump; J. Jung; T. Chao; R. Gupta M. Lin; P. Hahn; J. Kang; D. Frump; J. Jung; T. Chao; R. Gupta M. Lin; P. Hahn; J. Kang; D. Frump; J. Jung; T. Chao; R. Gupta

P-3 Efficacy Of C3 Peptide To Promote Peripheral Nerve Regeneration Depends On P-3 Efficacy Of C3 Peptide To Promote Peripheral Nerve Regeneration Depends On P-3 Efficacy Of C3 Peptide To Promote Peripheral Nerve Regeneration Depends On The Mode Of Application. The Mode Of Application. The Mode Of Application. K. Haastert-Talini, T. Hettwer, A. Rohrbeck, I. Just, C. Grothe K. Haastert-Talini, T. Hettwer, A. Rohrbeck, I. Just, C. Grothe K. Haastert-Talini, T. Hettwer, A. Rohrbeck, I. Just, C. Grothe

P-4 Peripheral Nerve Repair: An In Vivo Investigation of Structurally Enhanced P-4 Peripheral Nerve Repair: An In Vivo Investigation of Structurally Enhanced P-4 Peripheral Nerve Repair: An In Vivo Investigation of Structurally Enhanced Nerve Guidance Conduits Nerve Guidance Conduits Nerve Guidance Conduits W. Daly, M. Abu-Rub, B. Breen, D. Zeugolis, C. O’Connell, L. Yao, T.Windebank, W. Daly, M. Abu-Rub, B. Breen, D. Zeugolis, C. O’Connell, L. Yao, T.Windebank, W. Daly, M. Abu-Rub, B. Breen, D. Zeugolis, C. O’Connell, L. Yao, T.Windebank, A. Pandit A. Pandit A. Pandit

P-5 Mmp-3 Inhibition Blocks Degradation of The Neuromuscular Junction After P-5 Mmp-3 Inhibition Blocks Degradation of The Neuromuscular Junction After P-5 Mmp-3 Inhibition Blocks Degradation of The Neuromuscular Junction After Traumatic Peripheral Nerve Injury Traumatic Peripheral Nerve Injury Traumatic Peripheral Nerve Injury T. Chao; D. Frump; N. Nassiri; J. Jung; P. Hahn; T. Mozaffar; R. Gupta T. Chao; D. Frump; N. Nassiri; J. Jung; P. Hahn; T. Mozaffar; R. Gupta T. Chao; D. Frump; N. Nassiri; J. Jung; P. Hahn; T. Mozaffar; R. Gupta

P-6 Sensory Neuron Responses to Peripheral Tissue-Damage: Implications for SCI P-6 Sensory Neuron Responses to Peripheral Tissue-Damage: Implications for SCI P-6 Sensory Neuron Responses to Peripheral Tissue-Damage: Implications for SCI Secondary Conditions Secondary Conditions Secondary Conditions J.C. Petruska, C.H. Hill, K.K. Rau J.C. Petruska, C.H. Hill, K.K. Rau J.C. Petruska, C.H. Hill, K.K. Rau

P-7 Aspartate Aminotransferase Is Elevated In Rat Dorsal Root Ganglion Neurons P-7 Aspartate Aminotransferase Is Elevated In Rat Dorsal Root Ganglion Neurons P-7 Aspartate Aminotransferase Is Elevated In Rat Dorsal Root Ganglion Neurons During Regeneration Following Sciatic Nerve Crush During Regeneration Following Sciatic Nerve Crush During Regeneration Following Sciatic Nerve Crush B. Bolt, Z. Zhang, S. Alothman, K.E. Miller B. Bolt, Z. Zhang, S. Alothman, K.E. Miller B. Bolt, Z. Zhang, S. Alothman, K.E. Miller

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 25 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 25 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 25 OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

P-8 Vesicular Glutamate Transporter 2 Expression Is Altered In Dorsal Root Ganglion P-8 Vesicular Glutamate Transporter 2 Expression Is Altered In Dorsal Root Ganglion P-8 Vesicular Glutamate Transporter 2 Expression Is Altered In Dorsal Root Ganglion Neurons During The Regenerative Phase Following Sciatic Nerve Crush Neurons During The Regenerative Phase Following Sciatic Nerve Crush Neurons During The Regenerative Phase Following Sciatic Nerve Crush S. Alothman, Z. Zhang, B. Bolt, K.E. Miller S. Alothman, Z. Zhang, B. Bolt, K.E. Miller S. Alothman, Z. Zhang, B. Bolt, K.E. Miller

P-9 Alteration of Glutaminase In Rat Dorsal Root Ganglion Neurons During The P-9 Alteration of Glutaminase In Rat Dorsal Root Ganglion Neurons During The P-9 Alteration of Glutaminase In Rat Dorsal Root Ganglion Neurons During The Regenerative Phase Following Sciatic Nerve Crush Regenerative Phase Following Sciatic Nerve Crush Regenerative Phase Following Sciatic Nerve Crush Z. Zhang, S. Alothman, B. Bolt, K.E. Miller Z. Zhang, S. Alothman, B. Bolt, K.E. Miller Z. Zhang, S. Alothman, B. Bolt, K.E. Miller

P-10 An Immunohistochemical Analysis of Various Growth-Associated Proteins In P-10 An Immunohistochemical Analysis of Various Growth-Associated Proteins In P-10 An Immunohistochemical Analysis of Various Growth-Associated Proteins In Regenerating Adult Rat Retinal Ganglion Cells Regenerating Adult Rat Retinal Ganglion Cells Regenerating Adult Rat Retinal Ganglion Cells A.R. Harvey, C.E. Humphries, A.T. Julian, K.L. Hoath, M. Hellström, Y. Hu, M.A. A.R. Harvey, C.E. Humphries, A.T. Julian, K.L. Hoath, M. Hellström, Y. Hu, M.A. A.R. Harvey, C.E. Humphries, A.T. Julian, K.L. Hoath, M. Hellström, Y. Hu, M.A. Pollett Pollett Pollett

P-11 Patterns From Noise: A Data-Intensive Retrospective Study of Thoracic SCI P-11 Patterns From Noise: A Data-Intensive Retrospective Study of Thoracic SCI P-11 Patterns From Noise: A Data-Intensive Retrospective Study of Thoracic SCI Laboratory Records From 1992-2003 (N = 1400) Laboratory Records From 1992-2003 (N = 1400) Laboratory Records From 1992-2003 (N = 1400) A. R. Ferguson, C. F. Guandique, A. W. Liu, J. L. Nielson, J. C. Bresnahan, M. S. A. R. Ferguson, C. F. Guandique, A. W. Liu, J. L. Nielson, J. C. Bresnahan, M. S. A. R. Ferguson, C. F. Guandique, A. W. Liu, J. L. Nielson, J. C. Bresnahan, M. S. Beattie Beattie Beattie

P-12 Signals From Noise: Reflex Variability Analysis As A Diagnostic Tool In Spinal P-12 Signals From Noise: Reflex Variability Analysis As A Diagnostic Tool In Spinal P-12 Signals From Noise: Reflex Variability Analysis As A Diagnostic Tool In Spinal Cord Injury Cord Injury Cord Injury J.J. Cragg, L.M. Ramer, A.P. van Stolk, and M.S. Ramer J.J. Cragg, L.M. Ramer, A.P. van Stolk, and M.S. Ramer J.J. Cragg, L.M. Ramer, A.P. van Stolk, and M.S. Ramer

P-13 Evaluation Of Conduction Through Motor Pathways: Using Evoked Potentials In P-13 Evaluation Of Conduction Through Motor Pathways: Using Evoked Potentials In P-13 Evaluation Of Conduction Through Motor Pathways: Using Evoked Potentials In Non-Human Primates Non-Human Primates Non-Human Primates F. Benavides, D. Tovar, A. Santamaria, L. Guada, J. Guest F. Benavides, D. Tovar, A. Santamaria, L. Guada, J. Guest F. Benavides, D. Tovar, A. Santamaria, L. Guada, J. Guest

P-14 Correlates of Motor Dysfunction After Spinal Cord Injury In Rats P-14 Correlates of Motor Dysfunction After Spinal Cord Injury In Rats P-14 Correlates of Motor Dysfunction After Spinal Cord Injury In Rats G. Stein, J. Ankerne, O. Semler, S. Angelova, M. Ashrafi, L. Eisel, R. Harrach, G. G. Stein, J. Ankerne, O. Semler, S. Angelova, M. Ashrafi, L. Eisel, R. Harrach, G. G. Stein, J. Ankerne, O. Semler, S. Angelova, M. Ashrafi, L. Eisel, R. Harrach, G. Schempf, K. Wellmann, F. Wirth, O. Ozsoy, U. Ozsoy, E. Schönau, A. Irintchev, Schempf, K. Wellmann, F. Wirth, O. Ozsoy, U. Ozsoy, E. Schönau, A. Irintchev, Schempf, K. Wellmann, F. Wirth, O. Ozsoy, U. Ozsoy, E. Schönau, A. Irintchev, D. Angelov D. Angelov D. Angelov

P-15 Neuromuscular Plasticity In The Rat Forelimb After High Cervical Spinal Cord P-15 Neuromuscular Plasticity In The Rat Forelimb After High Cervical Spinal Cord P-15 Neuromuscular Plasticity In The Rat Forelimb After High Cervical Spinal Cord Injury Injury Injury E.J. Gonzalez-Rothi, R.A Federico, A. Daly, A. Rombola, B.E. O’Steen, E.J. Gonzalez-Rothi, R.A Federico, A. Daly, A. Rombola, B.E. O’Steen, E.J. Gonzalez-Rothi, R.A Federico, A. Daly, A. Rombola, B.E. O’Steen, K.V. Vandenborne, P.J. Reier, D.D. Fuller, M.A. Lane K.V. Vandenborne, P.J. Reier, D.D. Fuller, M.A. Lane K.V. Vandenborne, P.J. Reier, D.D. Fuller, M.A. Lane

P-16 In Vivo Testing Of Candidate Genes To Promote Neuron-Intrinsic Growth Ability P-16 In Vivo Testing Of Candidate Genes To Promote Neuron-Intrinsic Growth Ability P-16 In Vivo Testing Of Candidate Genes To Promote Neuron-Intrinsic Growth Ability And Axon Regeneration In The Injured Spinal Cord And Axon Regeneration In The Injured Spinal Cord And Axon Regeneration In The Injured Spinal Cord M.G. Blackmore, Z. Wang, P. Zheng, C. Shields, V.P. Lemmon, J.L. Bixby M.G. Blackmore, Z. Wang, P. Zheng, C. Shields, V.P. Lemmon, J.L. Bixby M.G. Blackmore, Z. Wang, P. Zheng, C. Shields, V.P. Lemmon, J.L. Bixby

P-17 Allogeneic And Autologous Schwann Cell Grafts In A Porcine SCI Contusion P-17 Allogeneic And Autologous Schwann Cell Grafts In A Porcine SCI Contusion P-17 Allogeneic And Autologous Schwann Cell Grafts In A Porcine SCI Contusion Model: Immune Response And CNS Integration Model: Immune Response And CNS Integration Model: Immune Response And CNS Integration A. Santamaria, F. Benavides, L. Guada, G. Athauda, H. Levene, J. Solano, J. A. Santamaria, F. Benavides, L. Guada, G. Athauda, H. Levene, J. Solano, J. A. Santamaria, F. Benavides, L. Guada, G. Athauda, H. Levene, J. Solano, J. Guest Guest Guest

26 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 26 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 26 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

P-18 Hot ‘n‘ bothered: the role of TRPV1-positive sensory neurons in autonomic P-18 Hot ‘n‘ bothered: the role of TRPV1-positive sensory neurons in autonomic P-18 Hot ‘n‘ bothered: the role of TRPV1-positive sensory neurons in autonomic dysreflexia dysreflexia dysreflexia L. M. Ramer, A. P. van Stolk, J. A. Inskip, M. S. Ramer, J. D. Steeves, A. V. L. M. Ramer, A. P. van Stolk, J. A. Inskip, M. S. Ramer, J. D. Steeves, A. V. L. M. Ramer, A. P. van Stolk, J. A. Inskip, M. S. Ramer, J. D. Steeves, A. V. Krassioukov Krassioukov Krassioukov

P-19 Myelin Gene Regulatory Factor Knockout Delays Functional Recovery From P-19 Myelin Gene Regulatory Factor Knockout Delays Functional Recovery From P-19 Myelin Gene Regulatory Factor Knockout Delays Functional Recovery From Spinal Cord Injury Spinal Cord Injury Spinal Cord Injury G. J. Duncan, J. R. Plemel, B. J. Hilton, J. Liu, J. K. Kramer, J. Kim, S. Mao, and G. J. Duncan, J. R. Plemel, B. J. Hilton, J. Liu, J. K. Kramer, J. Kim, S. Mao, and G. J. Duncan, J. R. Plemel, B. J. Hilton, J. Liu, J. K. Kramer, J. Kim, S. Mao, and W. Tetzlaff. W. Tetzlaff. W. Tetzlaff.

P-20 In Vivo Real Time Observations of Immune Cells And Neurons In Traumatic P-20 In Vivo Real Time Observations of Immune Cells And Neurons In Traumatic P-20 In Vivo Real Time Observations of Immune Cells And Neurons In Traumatic Spinal Cord Injury In The Mouse Spinal Cord Injury In The Mouse Spinal Cord Injury In The Mouse T. A. Evans, D. S. Barkauskas, A. Y. Huang, J. Silver T. A. Evans, D. S. Barkauskas, A. Y. Huang, J. Silver T. A. Evans, D. S. Barkauskas, A. Y. Huang, J. Silver

P-21 The Presence of Cd4+ T Cells Is Required For Nt-3-Induced Axonal Sprouting In P-21 The Presence of Cd4+ T Cells Is Required For Nt-3-Induced Axonal Sprouting In P-21 The Presence of Cd4+ T Cells Is Required For Nt-3-Induced Axonal Sprouting In The Injured Spinal Cord The Injured Spinal Cord The Injured Spinal Cord Q. Chen and H.D. Shine Q. Chen and H.D. Shine Q. Chen and H.D. Shine

P-22 Characterizing The Effect Of Neurotrauma On Spinal Cord And Dorsal Root P-22 Characterizing The Effect Of Neurotrauma On Spinal Cord And Dorsal Root P-22 Characterizing The Effect Of Neurotrauma On Spinal Cord And Dorsal Root Ganglion Vasculature Ganglion Vasculature Ganglion Vasculature M.A. Crawford and M.S. Ramer M.A. Crawford and M.S. Ramer M.A. Crawford and M.S. Ramer

P-23 Autonomic And Sensorimotor Recovery From Cervical Contusion Injury Is P-23 Autonomic And Sensorimotor Recovery From Cervical Contusion Injury Is P-23 Autonomic And Sensorimotor Recovery From Cervical Contusion Injury Is Boosted By Midbrain Periaqueductal Gray Stimulation. Boosted By Midbrain Periaqueductal Gray Stimulation. Boosted By Midbrain Periaqueductal Gray Stimulation. I.D. Hentall, A. Vitores, M.M. Carballosa-Gonzalez I.D. Hentall, A. Vitores, M.M. Carballosa-Gonzalez I.D. Hentall, A. Vitores, M.M. Carballosa-Gonzalez

P-24 Skin-Derived Precursors Differentiated Into Schwann Cells (Skp-Scs) And P-24 Skin-Derived Precursors Differentiated Into Schwann Cells (Skp-Scs) And P-24 Skin-Derived Precursors Differentiated Into Schwann Cells (Skp-Scs) And Transplanted Eight Weeks Post Spinal Cord Contusion Improve Recovery Of Transplanted Eight Weeks Post Spinal Cord Contusion Improve Recovery Of Transplanted Eight Weeks Post Spinal Cord Contusion Improve Recovery Of Motor Function And Bladder Pathology Motor Function And Bladder Pathology Motor Function And Bladder Pathology P. Assinck, S. Dworski, J.S. Sparling, G.J. Duncan, D.L. Wu, Y. Jiang, J. Liu, P. Assinck, S. Dworski, J.S. Sparling, G.J. Duncan, D.L. Wu, Y. Jiang, J. Liu, P. Assinck, S. Dworski, J.S. Sparling, G.J. Duncan, D.L. Wu, Y. Jiang, J. Liu, C.K. Lam, B.K. Kwon, F. D. Miller, W. Tetzlaff C.K. Lam, B.K. Kwon, F. D. Miller, W. Tetzlaff C.K. Lam, B.K. Kwon, F. D. Miller, W. Tetzlaff

P-25 Nerve Regeneration And Improvement In Urodynamics And External Urethral P-25 Nerve Regeneration And Improvement In Urodynamics And External Urethral P-25 Nerve Regeneration And Improvement In Urodynamics And External Urethral Sphincter Activity In Complete Spinal Cord Transected Rats Treated With A Sphincter Activity In Complete Spinal Cord Transected Rats Treated With A Sphincter Activity In Complete Spinal Cord Transected Rats Treated With A Peripheral Nerve Graft, Acidic Fibroblast Growth Factor, And Chondroitinase Peripheral Nerve Graft, Acidic Fibroblast Growth Factor, And Chondroitinase Peripheral Nerve Graft, Acidic Fibroblast Growth Factor, And Chondroitinase ABC ABC ABC Y.-S. Lee, H-H. Jiang, M. DePaul, C.-Y. Lin, M. S. Damaser, V. W. Lin, and J. Y.-S. Lee, H-H. Jiang, M. DePaul, C.-Y. Lin, M. S. Damaser, V. W. Lin, and J. Y.-S. Lee, H-H. Jiang, M. DePaul, C.-Y. Lin, M. S. Damaser, V. W. Lin, and J. Silver Silver Silver

P-26 Early and late behavioral and electrophysiological changes in lower urinary tract P-26 Early and late behavioral and electrophysiological changes in lower urinary tract P-26 Early and late behavioral and electrophysiological changes in lower urinary tract function following mid-cervical spinal cord injury function following mid-cervical spinal cord injury function following mid-cervical spinal cord injury T. Martin – Carreras, G. Grossl, D.D. Fuller, P.J Reier, M.A. Lane, D.J. Hoh T. Martin – Carreras, G. Grossl, D.D. Fuller, P.J Reier, M.A. Lane, D.J. Hoh T. Martin – Carreras, G. Grossl, D.D. Fuller, P.J Reier, M.A. Lane, D.J. Hoh

P-27 Integration of Microchannel Neural-Electrode Interfaces Into Dorsal And Ventral P-27 Integration of Microchannel Neural-Electrode Interfaces Into Dorsal And Ventral P-27 Integration of Microchannel Neural-Electrode Interfaces Into Dorsal And Ventral Roots For Bladder Control After Spinal Cord Injury Roots For Bladder Control After Spinal Cord Injury Roots For Bladder Control After Spinal Cord Injury

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 27 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 27 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 27 OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

D Chew, E Delivopoulos, N Granger, S Mosse, I Minev, L Zhu, S McMahon, M D Chew, E Delivopoulos, N Granger, S Mosse, I Minev, L Zhu, S McMahon, M D Chew, E Delivopoulos, N Granger, S Mosse, I Minev, L Zhu, S McMahon, M Craggs, N Jeffery, N Donaldson, S Lacour, J Fawcett Craggs, N Jeffery, N Donaldson, S Lacour, J Fawcett Craggs, N Jeffery, N Donaldson, S Lacour, J Fawcett

P-28 Optimized acellular Grafts Support Functional Recovery after Cervical Spinal P-28 Optimized acellular Grafts Support Functional Recovery after Cervical Spinal P-28 Optimized acellular Grafts Support Functional Recovery after Cervical Spinal Cord Injury Cord Injury Cord Injury Z. Z. Khaing, W. J. Alilain, J. Silver, and C. E. Schmidt Z. Z. Khaing, W. J. Alilain, J. Silver, and C. E. Schmidt Z. Z. Khaing, W. J. Alilain, J. Silver, and C. E. Schmidt

P-29 Environmental Enrichment Enhances Retrograde Transport of Polysynaptic P-29 Environmental Enrichment Enhances Retrograde Transport of Polysynaptic P-29 Environmental Enrichment Enhances Retrograde Transport of Polysynaptic Virus In The Dentate Gyrus After Traumatic Brain Injury Virus In The Dentate Gyrus After Traumatic Brain Injury Virus In The Dentate Gyrus After Traumatic Brain Injury C. Burger, R. Zamanskaya, W. Liu, T.-J. Chang, J. Liu C. Burger, R. Zamanskaya, W. Liu, T.-J. Chang, J. Liu C. Burger, R. Zamanskaya, W. Liu, T.-J. Chang, J. Liu

P-30 Analysis of Gene Expression Following A Localized Traumatic Brain Injury P-30 Analysis of Gene Expression Following A Localized Traumatic Brain Injury P-30 Analysis of Gene Expression Following A Localized Traumatic Brain Injury Reveals A Bias Toward Increased Cell Death Locally And Cell Survival Reveals A Bias Toward Increased Cell Death Locally And Cell Survival Reveals A Bias Toward Increased Cell Death Locally And Cell Survival Remotely Remotely Remotely T. E. White, G. D. Ford, A. Gates, M. LaPlaca, B. D. Ford T. E. White, G. D. Ford, A. Gates, M. LaPlaca, B. D. Ford T. E. White, G. D. Ford, A. Gates, M. LaPlaca, B. D. Ford

P-31 Training of The Impaired Forelimb After Traumatic Brain Injury Enhances P-31 Training of The Impaired Forelimb After Traumatic Brain Injury Enhances P-31 Training of The Impaired Forelimb After Traumatic Brain Injury Enhances Hippocampal Neurogenesis In Mice Without Corpus Callosum Hippocampal Neurogenesis In Mice Without Corpus Callosum Hippocampal Neurogenesis In Mice Without Corpus Callosum S. Wu, M. Neumann, W. Liu, C.C. Lee, R. Zamanskaya, L. Noble-Haeusslein and S. Wu, M. Neumann, W. Liu, C.C. Lee, R. Zamanskaya, L. Noble-Haeusslein and S. Wu, M. Neumann, W. Liu, C.C. Lee, R. Zamanskaya, L. Noble-Haeusslein and J. Liu J. Liu J. Liu

P-32 Using Multimodel Therapies To Improve Outcome Following Traumatic Brain P-32 Using Multimodel Therapies To Improve Outcome Following Traumatic Brain P-32 Using Multimodel Therapies To Improve Outcome Following Traumatic Brain Injury Injury Injury D. Bingham, T. Lam, J. Lee, T.J. Chang, C. Burger, C. Sun, S. Wu, J. Shi, S. D. Bingham, T. Lam, J. Lee, T.J. Chang, C. Burger, C. Sun, S. Wu, J. Shi, S. D. Bingham, T. Lam, J. Lee, T.J. Chang, C. Burger, C. Sun, S. Wu, J. Shi, S. Massa, R. A. Swanson, J. Liu. Massa, R. A. Swanson, J. Liu. Massa, R. A. Swanson, J. Liu.

P-33 Stroke Affects Functional Activation During Spatial Tasks P-33 Stroke Affects Functional Activation During Spatial Tasks P-33 Stroke Affects Functional Activation During Spatial Tasks S. Badurek, W. Liu, C. Burger, C. Lee, R. Saloner, J. Liu S. Badurek, W. Liu, C. Burger, C. Lee, R. Saloner, J. Liu S. Badurek, W. Liu, C. Burger, C. Lee, R. Saloner, J. Liu

P-34 Reduction of Neuroprogenitor Cells In Mice Impedes Post-Stroke Functional P-34 Reduction of Neuroprogenitor Cells In Mice Impedes Post-Stroke Functional P-34 Reduction of Neuroprogenitor Cells In Mice Impedes Post-Stroke Functional Recovery Recovery Recovery C. Sun, H. Sun, S. Wu, T.J. Chang, R. Saloner, S.G. Kernie and J. Liu C. Sun, H. Sun, S. Wu, T.J. Chang, R. Saloner, S.G. Kernie and J. Liu C. Sun, H. Sun, S. Wu, T.J. Chang, R. Saloner, S.G. Kernie and J. Liu

P-35 Experimental ischemic and hemorrhagic strokes induce memory impairment and P-35 Experimental ischemic and hemorrhagic strokes induce memory impairment and P-35 Experimental ischemic and hemorrhagic strokes induce memory impairment and reduce hippocampal functional recruitment during spatial navigation reduce hippocampal functional recruitment during spatial navigation reduce hippocampal functional recruitment during spatial navigation C.C.J. Lee, Y. Wang, W. Liu, C. Sun, S. Badurek, S. Wu, C. Burger, J. Liu C.C.J. Lee, Y. Wang, W. Liu, C. Sun, S. Badurek, S. Wu, C. Burger, J. Liu C.C.J. Lee, Y. Wang, W. Liu, C. Sun, S. Badurek, S. Wu, C. Burger, J. Liu

P-36 Unexpected Neuronal Loss After Spinal Cord Injections In Primates P-36 Unexpected Neuronal Loss After Spinal Cord Injections In Primates P-36 Unexpected Neuronal Loss After Spinal Cord Injections In Primates E. S. Rosenzweig, G. Courtine, J. H. Brock, Y. S. Nout, A. R. Ferguson, J. L. E. S. Rosenzweig, G. Courtine, J. H. Brock, Y. S. Nout, A. R. Ferguson, J. L. E. S. Rosenzweig, G. Courtine, J. H. Brock, Y. S. Nout, A. R. Ferguson, J. L. Nielson, S. C. Strand, R. Moseanko, S. Hawbecker, R. R. Roy, H. Zhong, J. L. Nielson, S. C. Strand, R. Moseanko, S. Hawbecker, R. R. Roy, H. Zhong, J. L. Nielson, S. C. Strand, R. Moseanko, S. Hawbecker, R. R. Roy, H. Zhong, J. L. Weber, M. S. Beattie, L. A. Havton, V. R. Edgerton, J. C. Bresnahan, O. Steward, Weber, M. S. Beattie, L. A. Havton, V. R. Edgerton, J. C. Bresnahan, O. Steward, Weber, M. S. Beattie, L. A. Havton, V. R. Edgerton, J. C. Bresnahan, O. Steward, and M. H. Tuszynski and M. H. Tuszynski and M. H. Tuszynski

P-37 Long-Distance Axonal Growth, Connectivity and Functional Recovery After P-37 Long-Distance Axonal Growth, Connectivity and Functional Recovery After P-37 Long-Distance Axonal Growth, Connectivity and Functional Recovery After Complete Spinal Cord Transection: Cell-Intrinsic Mechanisms Overcome Complete Spinal Cord Transection: Cell-Intrinsic Mechanisms Overcome Complete Spinal Cord Transection: Cell-Intrinsic Mechanisms Overcome Inhibition Of The Adult Lesioned Spinal Cord Inhibition Of The Adult Lesioned Spinal Cord Inhibition Of The Adult Lesioned Spinal Cord

28 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 28 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 28 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

J.H. Brock, P. Lu, Y. Wang, L. Graham, K. McHale, M. Gao, D. Wu, , L.A. J.H. Brock, P. Lu, Y. Wang, L. Graham, K. McHale, M. Gao, D. Wu, , L.A. J.H. Brock, P. Lu, Y. Wang, L. Graham, K. McHale, M. Gao, D. Wu, , L.A. Havton, A. Blesch, B. Zheng, J.M. Conner, and M.H. Tuszynski Havton, A. Blesch, B. Zheng, J.M. Conner, and M.H. Tuszynski Havton, A. Blesch, B. Zheng, J.M. Conner, and M.H. Tuszynski

P-38 Daily Acute Intermittent Hypoxia Restores Respiratory Plasticity And Breathing P-38 Daily Acute Intermittent Hypoxia Restores Respiratory Plasticity And Breathing P-38 Daily Acute Intermittent Hypoxia Restores Respiratory Plasticity And Breathing Capacity Following Cervical Injury Capacity Following Cervical Injury Capacity Following Cervical Injury S. Vinit, J. Terada, P.M. MacFarlane, G.S. Mitchell S. Vinit, J. Terada, P.M. MacFarlane, G.S. Mitchell S. Vinit, J. Terada, P.M. MacFarlane, G.S. Mitchell

P-39 Molecular Mechanisms involved in Recovery of Respiration after Upper cervical P-39 Molecular Mechanisms involved in Recovery of Respiration after Upper cervical P-39 Molecular Mechanisms involved in Recovery of Respiration after Upper cervical Spinal Cord Injury: Potential Therapeutic Strategies. Spinal Cord Injury: Potential Therapeutic Strategies. Spinal Cord Injury: Potential Therapeutic Strategies. K. D. Nantwi, and L. P. Singh K. D. Nantwi, and L. P. Singh K. D. Nantwi, and L. P. Singh

P-40 Intraspinal grafts of neural progenitors improves respiratory function following P-40 Intraspinal grafts of neural progenitors improves respiratory function following P-40 Intraspinal grafts of neural progenitors improves respiratory function following mid-cervical contusion injury in adult rats mid-cervical contusion injury in adult rats mid-cervical contusion injury in adult rats D.E. Sanchez, K. Salazar, L.M. Mercier, B.E. O’Steen, P.J. Reier, M.A. Lane D.E. Sanchez, K. Salazar, L.M. Mercier, B.E. O’Steen, P.J. Reier, M.A. Lane D.E. Sanchez, K. Salazar, L.M. Mercier, B.E. O’Steen, P.J. Reier, M.A. Lane

P-41 Changes In Interneuronal Activity In The Cervical Spinal Cord Of Adult Rats P-41 Changes In Interneuronal Activity In The Cervical Spinal Cord Of Adult Rats P-41 Changes In Interneuronal Activity In The Cervical Spinal Cord Of Adult Rats Following Spinal Cord Injury (SCI) Following Spinal Cord Injury (SCI) Following Spinal Cord Injury (SCI) V.M. Spruance, A.M. Rombola, B.E. O’Steen, M.A. Lane, P.J. Reier V.M. Spruance, A.M. Rombola, B.E. O’Steen, M.A. Lane, P.J. Reier V.M. Spruance, A.M. Rombola, B.E. O’Steen, M.A. Lane, P.J. Reier

P-42 High Cervical Spinal Cord Injury Results In Altered Distributions of Medullary P-42 High Cervical Spinal Cord Injury Results In Altered Distributions of Medullary P-42 High Cervical Spinal Cord Injury Results In Altered Distributions of Medullary Inspiratory And Expiratory Neuronal Activity Inspiratory And Expiratory Neuronal Activity Inspiratory And Expiratory Neuronal Activity L.M. Mercier, D.F. Ryczek, K-Z Lee, B.E. O’Steen, D.D. Fuller, P.J. Reier, M.A. L.M. Mercier, D.F. Ryczek, K-Z Lee, B.E. O’Steen, D.D. Fuller, P.J. Reier, M.A. L.M. Mercier, D.F. Ryczek, K-Z Lee, B.E. O’Steen, D.D. Fuller, P.J. Reier, M.A. Lane Lane Lane

P-43 Synaptic Integration of Transplanted Cells With Phrenic Circuitry Following P-43 Synaptic Integration of Transplanted Cells With Phrenic Circuitry Following P-43 Synaptic Integration of Transplanted Cells With Phrenic Circuitry Following High Cervical Spinal Cord Injury In Adult Rat High Cervical Spinal Cord Injury In Adult Rat High Cervical Spinal Cord Injury In Adult Rat C. Lopez, J. Loftus, E.J. Gonzalez-Rothi, L.M. Mercier, A.M. Rombola, B.E. C. Lopez, J. Loftus, E.J. Gonzalez-Rothi, L.M. Mercier, A.M. Rombola, B.E. C. Lopez, J. Loftus, E.J. Gonzalez-Rothi, L.M. Mercier, A.M. Rombola, B.E. O’Steen, D.D. Fuller, M.A. Lane, P.J. Reier O’Steen, D.D. Fuller, M.A. Lane, P.J. Reier O’Steen, D.D. Fuller, M.A. Lane, P.J. Reier

P-44 Persistent Diaphragm Dysfunction Following Lateralized Cervical Contusion P-44 Persistent Diaphragm Dysfunction Following Lateralized Cervical Contusion P-44 Persistent Diaphragm Dysfunction Following Lateralized Cervical Contusion S. Hussey, D.E. Sanchez, B.E Osteen, D.D. Fuller, M.A. Lane, P.J Reier S. Hussey, D.E. Sanchez, B.E Osteen, D.D. Fuller, M.A. Lane, P.J Reier S. Hussey, D.E. Sanchez, B.E Osteen, D.D. Fuller, M.A. Lane, P.J Reier

P-45 Chondroitinase ABC Treatment And Modest Exposure To Intermittent Hypoxia P-45 Chondroitinase ABC Treatment And Modest Exposure To Intermittent Hypoxia P-45 Chondroitinase ABC Treatment And Modest Exposure To Intermittent Hypoxia Restores Hemidiaphragmatic Activity After Cervical Spinal Cord Injury Restores Hemidiaphragmatic Activity After Cervical Spinal Cord Injury Restores Hemidiaphragmatic Activity After Cervical Spinal Cord Injury W.J. Alilain, M. Clark, J. Silver W.J. Alilain, M. Clark, J. Silver W.J. Alilain, M. Clark, J. Silver

P-46 Ipsilateral Inspiratory Intercostal Muscle Activity After C2 Spinal Cord P-46 Ipsilateral Inspiratory Intercostal Muscle Activity After C2 Spinal Cord P-46 Ipsilateral Inspiratory Intercostal Muscle Activity After C2 Spinal Cord Hemisection Hemisection Hemisection M. B. Zimmer, J. Grant, A. Ayar and H. G. Goshgarian M. B. Zimmer, J. Grant, A. Ayar and H. G. Goshgarian M. B. Zimmer, J. Grant, A. Ayar and H. G. Goshgarian

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 29 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 29 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 29 OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

SESSION TWO SESSION TWO SESSION TWO

P-47 Generation of High Purity Neuronal Progenitor Cells And Oligodendrocyte P-47 Generation of High Purity Neuronal Progenitor Cells And Oligodendrocyte P-47 Generation of High Purity Neuronal Progenitor Cells And Oligodendrocyte Progenitor Cells From Blastocyst-Derived Human Embryonic Stem Cells And Progenitor Cells From Blastocyst-Derived Human Embryonic Stem Cells And Progenitor Cells From Blastocyst-Derived Human Embryonic Stem Cells And Human Induced Pluripotent Stem Cells Human Induced Pluripotent Stem Cells Human Induced Pluripotent Stem Cells M. Wedemeyer, K. Stahl, D. Ferguson, J. Frame, C. Cruz, J. Harness, G. Nistor, M. Wedemeyer, K. Stahl, D. Ferguson, J. Frame, C. Cruz, J. Harness, G. Nistor, M. Wedemeyer, K. Stahl, D. Ferguson, J. Frame, C. Cruz, J. Harness, G. Nistor, H. Okano, S. Yamanaka, H. Keirstead H. Okano, S. Yamanaka, H. Keirstead H. Okano, S. Yamanaka, H. Keirstead

P-48 Characterization Of High Purity Neuronal Progenitors Isolated From Human P-48 Characterization Of High Purity Neuronal Progenitors Isolated From Human P-48 Characterization Of High Purity Neuronal Progenitors Isolated From Human Embryonic Stem Cells Embryonic Stem Cells Embryonic Stem Cells G. Nistor, A. Poole, M. Siegenthaler, J. Sharp, C. Fredrickson, C. Airriess, H. G. Nistor, A. Poole, M. Siegenthaler, J. Sharp, C. Fredrickson, C. Airriess, H. G. Nistor, A. Poole, M. Siegenthaler, J. Sharp, C. Fredrickson, C. Airriess, H. Keirstead Keirstead Keirstead

P-49 Developing A Human Drug Discovery Platform For Huntington’s Disease P-49 Developing A Human Drug Discovery Platform For Huntington’s Disease P-49 Developing A Human Drug Discovery Platform For Huntington’s Disease J.V. Harness, C. Armstrong, M. Evans, I. Soltesz, L. Thompson, H.S. Keirstead J.V. Harness, C. Armstrong, M. Evans, I. Soltesz, L. Thompson, H.S. Keirstead J.V. Harness, C. Armstrong, M. Evans, I. Soltesz, L. Thompson, H.S. Keirstead

P-50 High Purity Mouse Embryonic Stem Cell-Derived Progenitor Motor Neurons For P-50 High Purity Mouse Embryonic Stem Cell-Derived Progenitor Motor Neurons For P-50 High Purity Mouse Embryonic Stem Cell-Derived Progenitor Motor Neurons For Transplantation After Spinal Cord Injury Transplantation After Spinal Cord Injury Transplantation After Spinal Cord Injury D.A. McCreedy, C.R. Silverman, D.I. Gottliebb, S.E. Sakiyama-Elbert D.A. McCreedy, C.R. Silverman, D.I. Gottliebb, S.E. Sakiyama-Elbert D.A. McCreedy, C.R. Silverman, D.I. Gottliebb, S.E. Sakiyama-Elbert

P-51 The Effects of Human Motor Neuron Progenitor Transplants In A Mouse Model P-51 The Effects of Human Motor Neuron Progenitor Transplants In A Mouse Model P-51 The Effects of Human Motor Neuron Progenitor Transplants In A Mouse Model Of Spinal Muscular Atrophy Of Spinal Muscular Atrophy Of Spinal Muscular Atrophy T.J. Wyatt, S. Rossi, G. Nistor, A. Poole, M. Siegenthaler, H.S. Keirstead T.J. Wyatt, S. Rossi, G. Nistor, A. Poole, M. Siegenthaler, H.S. Keirstead T.J. Wyatt, S. Rossi, G. Nistor, A. Poole, M. Siegenthaler, H.S. Keirstead

P-52 Adult Spinal Cord Radial Glia Display A Unique Progenitor Phenotype P-52 Adult Spinal Cord Radial Glia Display A Unique Progenitor Phenotype P-52 Adult Spinal Cord Radial Glia Display A Unique Progenitor Phenotype A. Petit, A. D. Sanders, T. E. Kennedy, W. Tetzlaff, K. J. Glattfelder, R. A. Dalley, A. Petit, A. D. Sanders, T. E. Kennedy, W. Tetzlaff, K. J. Glattfelder, R. A. Dalley, A. Petit, A. D. Sanders, T. E. Kennedy, W. Tetzlaff, K. J. Glattfelder, R. A. Dalley, R. B. Puchalski, A. R. Jones, A. J. Roskams R. B. Puchalski, A. R. Jones, A. J. Roskams R. B. Puchalski, A. R. Jones, A. J. Roskams

P-53 Anatomical & Functional Characterization Of Fenestrated Endothelium P-53 Anatomical & Functional Characterization Of Fenestrated Endothelium P-53 Anatomical & Functional Characterization Of Fenestrated Endothelium Formation During Revascularization In The Injured Spinal Cord Formation During Revascularization In The Injured Spinal Cord Formation During Revascularization In The Injured Spinal Cord A.P. Montague, A. Ribble, C. Conrad, A.B. Mozer, and R.L. Benton. A.P. Montague, A. Ribble, C. Conrad, A.B. Mozer, and R.L. Benton. A.P. Montague, A. Ribble, C. Conrad, A.B. Mozer, and R.L. Benton.

P-54 Thrombin Inhbits Adult Neural Progenitor Integration And Regeneration By P-54 Thrombin Inhbits Adult Neural Progenitor Integration And Regeneration By P-54 Thrombin Inhbits Adult Neural Progenitor Integration And Regeneration By Promoting Astrogliogenesis Via Id1. Promoting Astrogliogenesis Via Id1. Promoting Astrogliogenesis Via Id1. D. L. Sellers, M. E. Gill, D. O. Maris, D. J. Calkins, P. J. Horner D. L. Sellers, M. E. Gill, D. O. Maris, D. J. Calkins, P. J. Horner D. L. Sellers, M. E. Gill, D. O. Maris, D. J. Calkins, P. J. Horner

P-55 Transplantation of Human Mpcs In Combination With Scar Reducing Decorin P-55 Transplantation of Human Mpcs In Combination With Scar Reducing Decorin P-55 Transplantation of Human Mpcs In Combination With Scar Reducing Decorin Following Acute And Chronic Spinal Cord Injury In The Rat. Following Acute And Chronic Spinal Cord Injury In The Rat. Following Acute And Chronic Spinal Cord Injury In The Rat. S.I. Hodgetts, P.J. Simmons, A. Buckley, G.W. Plant S.I. Hodgetts, P.J. Simmons, A. Buckley, G.W. Plant S.I. Hodgetts, P.J. Simmons, A. Buckley, G.W. Plant

P-56 Self-renewal and multipotential properties of GFAP-expressing cell populations P-56 Self-renewal and multipotential properties of GFAP-expressing cell populations P-56 Self-renewal and multipotential properties of GFAP-expressing cell populations in the adult spinal cord in the adult spinal cord in the adult spinal cord R. Fiorelli & O. Raineteau R. Fiorelli & O. Raineteau R. Fiorelli & O. Raineteau

30 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 30 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 30 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

P-57 Optimizing Recovery Of Overground Locomotion With Novel Robotic Gait P-57 Optimizing Recovery Of Overground Locomotion With Novel Robotic Gait P-57 Optimizing Recovery Of Overground Locomotion With Novel Robotic Gait Training Patterns Following SCI In Rats Training Patterns Following SCI In Rats Training Patterns Following SCI In Rats N.D. Neckel, H. Dai, J. Laracy, M. McAtee, C. Soper, B. Bregman N.D. Neckel, H. Dai, J. Laracy, M. McAtee, C. Soper, B. Bregman N.D. Neckel, H. Dai, J. Laracy, M. McAtee, C. Soper, B. Bregman

P-58 Robotic Training In Spinal Rats Produces Novel Gait Patterns And Abnormally P-58 Robotic Training In Spinal Rats Produces Novel Gait Patterns And Abnormally P-58 Robotic Training In Spinal Rats Produces Novel Gait Patterns And Abnormally High Levels Of Glutamate And Glycine In The Lumbar Spinal Cord High Levels Of Glutamate And Glycine In The Lumbar Spinal Cord High Levels Of Glutamate And Glycine In The Lumbar Spinal Cord P.A. See, E. Partida, M.J. Cantoria, H. Singh, R.D. de Leon P.A. See, E. Partida, M.J. Cantoria, H. Singh, R.D. de Leon P.A. See, E. Partida, M.J. Cantoria, H. Singh, R.D. de Leon

P-59 Dose Dependant Effects of BDNF on Locomotor Recovery In Paraplegic Rats P-59 Dose Dependant Effects of BDNF on Locomotor Recovery In Paraplegic Rats P-59 Dose Dependant Effects of BDNF on Locomotor Recovery In Paraplegic Rats V.S. Boyce, J. Park, F.H. Gage and L.M. Mendell V.S. Boyce, J. Park, F.H. Gage and L.M. Mendell V.S. Boyce, J. Park, F.H. Gage and L.M. Mendell

P-60 Post-Injury Administration of An Oxidoreductant Confers Protection After P-60 Post-Injury Administration of An Oxidoreductant Confers Protection After P-60 Post-Injury Administration of An Oxidoreductant Confers Protection After Contusional Spinal Cord Injury In Adult Rats Contusional Spinal Cord Injury In Adult Rats Contusional Spinal Cord Injury In Adult Rats K. Savage, M. Girard, H. M. Tse, C. L. Floyd K. Savage, M. Girard, H. M. Tse, C. L. Floyd K. Savage, M. Girard, H. M. Tse, C. L. Floyd

P-61 Fibronectin Administration Inhibits Chronic Pain Development After Spinal Cord P-61 Fibronectin Administration Inhibits Chronic Pain Development After Spinal Cord P-61 Fibronectin Administration Inhibits Chronic Pain Development After Spinal Cord Injury Injury Injury C.-Y. Lin, Y.-S. Lee, V. W. Lin, J. Silver C.-Y. Lin, Y.-S. Lee, V. W. Lin, J. Silver C.-Y. Lin, Y.-S. Lee, V. W. Lin, J. Silver

P-62 Every Move You Make: Consequences of A Stretching/ROM Therapy Post-SCI P-62 Every Move You Make: Consequences of A Stretching/ROM Therapy Post-SCI P-62 Every Move You Make: Consequences of A Stretching/ROM Therapy Post-SCI K.L. Caudle, D.A. Atkinson, A. Shum-Siu, D.S.K. Magnuson K.L. Caudle, D.A. Atkinson, A. Shum-Siu, D.S.K. Magnuson K.L. Caudle, D.A. Atkinson, A. Shum-Siu, D.S.K. Magnuson

P-63 Comparison Of The Effects Of Rubrospinal Tract And Red Nucleus Lesions On P-63 Comparison Of The Effects Of Rubrospinal Tract And Red Nucleus Lesions On P-63 Comparison Of The Effects Of Rubrospinal Tract And Red Nucleus Lesions On Skilled Reaching. Skilled Reaching. Skilled Reaching. R. Morris and A. Kearsley R. Morris and A. Kearsley R. Morris and A. Kearsley

P-64 PTEN Deletion Promotes Regenerative Sprouting In The Aged Rubrospinal Tract P-64 PTEN Deletion Promotes Regenerative Sprouting In The Aged Rubrospinal Tract P-64 PTEN Deletion Promotes Regenerative Sprouting In The Aged Rubrospinal Tract B.J. Hilton and W. Tetzlaff B.J. Hilton and W. Tetzlaff B.J. Hilton and W. Tetzlaff

P-65 Intra-Cortical Injection of AAV- shRNA Abrogates PTEN Expression In Cortical P-65 Intra-Cortical Injection of AAV- shRNA Abrogates PTEN Expression In Cortical P-65 Intra-Cortical Injection of AAV- shRNA Abrogates PTEN Expression In Cortical Motoneurons Motoneurons Motoneurons G. Lewandowski and O. Steward G. Lewandowski and O. Steward G. Lewandowski and O. Steward

P-66 Conditional Genetic Deletion of PTEN in the Sensorimotor Cortex Does Not P-66 Conditional Genetic Deletion of PTEN in the Sensorimotor Cortex Does Not P-66 Conditional Genetic Deletion of PTEN in the Sensorimotor Cortex Does Not Lead To Evident Motor Impairments Lead To Evident Motor Impairments Lead To Evident Motor Impairments K.G. Sharp, L.E. Butler, O. Steward K.G. Sharp, L.E. Butler, O. Steward K.G. Sharp, L.E. Butler, O. Steward

P-67 Long-Term Deletion of PTEN in the Sensorimotor Cortex Causes Neuronal P-67 Long-Term Deletion of PTEN in the Sensorimotor Cortex Causes Neuronal P-67 Long-Term Deletion of PTEN in the Sensorimotor Cortex Causes Neuronal Hypertrophy But Does Not Lead To Tumors Or Other Neuropathology Hypertrophy But Does Not Lead To Tumors Or Other Neuropathology Hypertrophy But Does Not Lead To Tumors Or Other Neuropathology M.M. Buyukozturk, B. Brandon, O. Steward M.M. Buyukozturk, B. Brandon, O. Steward M.M. Buyukozturk, B. Brandon, O. Steward

P-68 3D Imaging Of CST Axons That Regenerate After Spinal Cord Injury Due To P-68 3D Imaging Of CST Axons That Regenerate After Spinal Cord Injury Due To P-68 3D Imaging Of CST Axons That Regenerate After Spinal Cord Injury Due To PTEN Deletion PTEN Deletion PTEN Deletion R. Willenberg, A. Ertürk, F. Bradke, Z. He and O. Steward R. Willenberg, A. Ertürk, F. Bradke, Z. He and O. Steward R. Willenberg, A. Ertürk, F. Bradke, Z. He and O. Steward

P-69 TNFa-Induced AMPA Receptor Changes Undermine Adaptive Spinal Plasticity P-69 TNFa-Induced AMPA Receptor Changes Undermine Adaptive Spinal Plasticity P-69 TNFa-Induced AMPA Receptor Changes Undermine Adaptive Spinal Plasticity

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 31 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 31 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 31 OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

J.R. Huie, E.D. Stuck, K.H. Lee, J.C. Bresnahan, M.S. Beattie, J.W. Grau, A.R. J.R. Huie, E.D. Stuck, K.H. Lee, J.C. Bresnahan, M.S. Beattie, J.W. Grau, A.R. J.R. Huie, E.D. Stuck, K.H. Lee, J.C. Bresnahan, M.S. Beattie, J.W. Grau, A.R. Ferguson Ferguson Ferguson

P-70 An In Vitro Study Of The Roles Of Cspgs On Neurons: Neurite Outgrowth P-70 An In Vitro Study Of The Roles Of Cspgs On Neurons: Neurite Outgrowth P-70 An In Vitro Study Of The Roles Of Cspgs On Neurons: Neurite Outgrowth Inhibition Or Neuroprotection? Inhibition Or Neuroprotection? Inhibition Or Neuroprotection? P. Yu, Y. Katagiri, J. Yi, H.M. Geller P. Yu, Y. Katagiri, J. Yi, H.M. Geller P. Yu, Y. Katagiri, J. Yi, H.M. Geller

P-71 RPTP Demonstrates A Complex Pattern Of Binding To Proteoglycans P-71 RPTP Demonstrates A Complex Pattern Of Binding To Proteoglycans P-71 RPTP Demonstrates A Complex Pattern Of Binding To Proteoglycans Following Traumatic Brain Injury Following Traumatic Brain Injury Following Traumatic Brain Injury J. Yi, Y. Katagiri, A. J. Symes and H. M. Geller. J. Yi, Y. Katagiri, A. J. Symes and H. M. Geller. J. Yi, Y. Katagiri, A. J. Symes and H. M. Geller.

P-72 Reduction of CSPGs after Cortical Brain Injury Enhances Forelimb-Evoked Brain P-72 Reduction of CSPGs after Cortical Brain Injury Enhances Forelimb-Evoked Brain P-72 Reduction of CSPGs after Cortical Brain Injury Enhances Forelimb-Evoked Brain Activation Activation Activation M. Nogueira, D. Verley, D. Hovda, R. Sutton, N. Harris M. Nogueira, D. Verley, D. Hovda, R. Sutton, N. Harris M. Nogueira, D. Verley, D. Hovda, R. Sutton, N. Harris

P-73 Transient Expression And Purification Of Aggrecanase (Adamts-4) From P-73 Transient Expression And Purification Of Aggrecanase (Adamts-4) From P-73 Transient Expression And Purification Of Aggrecanase (Adamts-4) From Hek293t Cells Hek293t Cells Hek293t Cells J. Davies, D. M. Snow, and T. M. Hering J. Davies, D. M. Snow, and T. M. Hering J. Davies, D. M. Snow, and T. M. Hering

P-74 HEK293T Cells Produce Proteoglycans with Varied Sulfation Patterns, Express P-74 HEK293T Cells Produce Proteoglycans with Varied Sulfation Patterns, Express P-74 HEK293T Cells Produce Proteoglycans with Varied Sulfation Patterns, Express Multiple Carbohydrate Sulfotransferases, and are a Novel System for the Multiple Carbohydrate Sulfotransferases, and are a Novel System for the Multiple Carbohydrate Sulfotransferases, and are a Novel System for the Production of “Designer PGs”. Production of “Designer PGs”. Production of “Designer PGs”. J. A. Beller, T. M. Hering, D.M. Snow J. A. Beller, T. M. Hering, D.M. Snow J. A. Beller, T. M. Hering, D.M. Snow

P-75 Overlapping Yet Distinct Roles Of Matrix Metalloproteinases-2 And -9 In P-75 Overlapping Yet Distinct Roles Of Matrix Metalloproteinases-2 And -9 In P-75 Overlapping Yet Distinct Roles Of Matrix Metalloproteinases-2 And -9 In Modulating Angiogenesis In The Injured Spinal Cord Modulating Angiogenesis In The Injured Spinal Cord Modulating Angiogenesis In The Injured Spinal Cord A. A. Trivedi, H. Zhang, A. Ekeledo, S. M. Lee, Z. Werb, K. Topp and L. J. Noble- A. A. Trivedi, H. Zhang, A. Ekeledo, S. M. Lee, Z. Werb, K. Topp and L. J. Noble- A. A. Trivedi, H. Zhang, A. Ekeledo, S. M. Lee, Z. Werb, K. Topp and L. J. Noble- Haeusslein Haeusslein Haeusslein

P-76 Axonal Regrowth Is Regulated By Mrnas Competing For Zbp1. P-76 Axonal Regrowth Is Regulated By Mrnas Competing For Zbp1. P-76 Axonal Regrowth Is Regulated By Mrnas Competing For Zbp1. J.L. Twiss, C.J. Donnelly, M. Spillane, D.E. Willis, M. Park, M. Xu, S. Yoo, G.J. J.L. Twiss, C.J. Donnelly, M. Spillane, D.E. Willis, M. Park, M. Xu, S. Yoo, G.J. J.L. Twiss, C.J. Donnelly, M. Spillane, D.E. Willis, M. Park, M. Xu, S. Yoo, G.J. Bassell and G. Gallo. Bassell and G. Gallo. Bassell and G. Gallo.

P-77 The Pro-Synaptic Protein LAR Mediates Glial Scar Induced Axonal Regernation P-77 The Pro-Synaptic Protein LAR Mediates Glial Scar Induced Axonal Regernation P-77 The Pro-Synaptic Protein LAR Mediates Glial Scar Induced Axonal Regernation Failure Following Spinal Cord Injury Failure Following Spinal Cord Injury Failure Following Spinal Cord Injury B.T. Lang, J.M. Cregg, Y.L. Wang, S. Li and J. Silver B.T. Lang, J.M. Cregg, Y.L. Wang, S. Li and J. Silver B.T. Lang, J.M. Cregg, Y.L. Wang, S. Li and J. Silver

P-78 Bidirectional Remodeling Of 1-Integrin Adhesions During Chemotropic P-78 Bidirectional Remodeling Of 1-Integrin Adhesions During Chemotropic P-78 Bidirectional Remodeling Of 1-Integrin Adhesions During Chemotropic Regulation Of Nerve Growth Regulation Of Nerve Growth Regulation Of Nerve Growth L.P. Carlstrom, J.H. Hines, J.R. Henley L.P. Carlstrom, J.H. Hines, J.R. Henley L.P. Carlstrom, J.H. Hines, J.R. Henley

P-79 In Vivo 2 Photon Imaging Of CNS Injury In Nogo Deficient Mice P-79 In Vivo 2 Photon Imaging Of CNS Injury In Nogo Deficient Mice P-79 In Vivo 2 Photon Imaging Of CNS Injury In Nogo Deficient Mice A. Lorenzana, O. Ghassemi, B. Zheng A. Lorenzana, O. Ghassemi, B. Zheng A. Lorenzana, O. Ghassemi, B. Zheng

P-80 A Very Large Organelle in Sympathetic Neurons P-80 A Very Large Organelle in Sympathetic Neurons P-80 A Very Large Organelle in Sympathetic Neurons D.V. Hunter and M.S. Ramer D.V. Hunter and M.S. Ramer D.V. Hunter and M.S. Ramer

32 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 32 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 32 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS OVERVIEW - POSTER PRESENTATIONS

P-81 CD8+ T Cell Granzymes Injure Axons By Dysregulating Axonal Ionic P-81 CD8+ T Cell Granzymes Injure Axons By Dysregulating Axonal Ionic P-81 CD8+ T Cell Granzymes Injure Axons By Dysregulating Axonal Ionic Homeostasis Homeostasis Homeostasis B. M. Sauer, W. F. Schmastieg, C. L. Howe B. M. Sauer, W. F. Schmastieg, C. L. Howe B. M. Sauer, W. F. Schmastieg, C. L. Howe

P-82 Toll-Like Receptor 2 Activation Limits Axon Dieback In Vivo And Promotes P-82 Toll-Like Receptor 2 Activation Limits Axon Dieback In Vivo And Promotes P-82 Toll-Like Receptor 2 Activation Limits Axon Dieback In Vivo And Promotes Macrophage-Mediated Regeneration In Vitro Without Causing Concurrent Macrophage-Mediated Regeneration In Vitro Without Causing Concurrent Macrophage-Mediated Regeneration In Vitro Without Causing Concurrent Neurotoxicity Neurotoxicity Neurotoxicity J.C. Gensel, K.A. Beckwith, and P.G. Popovich J.C. Gensel, K.A. Beckwith, and P.G. Popovich J.C. Gensel, K.A. Beckwith, and P.G. Popovich

P-83 Reparative Effects Of Raphe-Spinal Activity Mediated By 5-Ht7 Receptors, P-83 Reparative Effects Of Raphe-Spinal Activity Mediated By 5-Ht7 Receptors, P-83 Reparative Effects Of Raphe-Spinal Activity Mediated By 5-Ht7 Receptors, Camp Signalling Cascade, And Co-Released Neuropeptides Camp Signalling Cascade, And Co-Released Neuropeptides Camp Signalling Cascade, And Co-Released Neuropeptides M. M. Carballosa Gonzalez, A. Vitores, A. Oliva, I.D. Hentall M. M. Carballosa Gonzalez, A. Vitores, A. Oliva, I.D. Hentall M. M. Carballosa Gonzalez, A. Vitores, A. Oliva, I.D. Hentall

P-84 Polymer Mediated Delivery Of Xylosyltransferase-I Sirna To Suppress Glial Scar P-84 Polymer Mediated Delivery Of Xylosyltransferase-I Sirna To Suppress Glial Scar P-84 Polymer Mediated Delivery Of Xylosyltransferase-I Sirna To Suppress Glial Scar Glycosaminoglycan Synthesis Glycosaminoglycan Synthesis Glycosaminoglycan Synthesis M. T. Abu-Rub, M. Naughton, B. Newland, N. Madigan, B. Breen, S. McMahon, M. T. Abu-Rub, M. Naughton, B. Newland, N. Madigan, B. Breen, S. McMahon, M. T. Abu-Rub, M. Naughton, B. Newland, N. Madigan, B. Breen, S. McMahon, W. Wang, A. Windebank, A. Pandit W. Wang, A. Windebank, A. Pandit W. Wang, A. Windebank, A. Pandit

P-85 Microtubule Stabilization Reduces Scarring And Causes Axon Regeneration After P-85 Microtubule Stabilization Reduces Scarring And Causes Axon Regeneration After P-85 Microtubule Stabilization Reduces Scarring And Causes Axon Regeneration After Spinal Cord Injury Spinal Cord Injury Spinal Cord Injury F. Hellal, A. Hurtado, J. Ruschel, K.C. Flynn, C.J. Laskowski, M. Umlauf, L.C. F. Hellal, A. Hurtado, J. Ruschel, K.C. Flynn, C.J. Laskowski, M. Umlauf, L.C. F. Hellal, A. Hurtado, J. Ruschel, K.C. Flynn, C.J. Laskowski, M. Umlauf, L.C. Kapitein, D. Strikis, V. Lemmon, J. Bixby, C.C. Hoogenraad, F. Bradke Kapitein, D. Strikis, V. Lemmon, J. Bixby, C.C. Hoogenraad, F. Bradke Kapitein, D. Strikis, V. Lemmon, J. Bixby, C.C. Hoogenraad, F. Bradke

P-86 Single Filopodial Contact With Inhibitory Chondroitin Sulfate Proteoglycans P-86 Single Filopodial Contact With Inhibitory Chondroitin Sulfate Proteoglycans P-86 Single Filopodial Contact With Inhibitory Chondroitin Sulfate Proteoglycans Induces Behavioral Changes In Sensory Neurons In Vitro Induces Behavioral Changes In Sensory Neurons In Vitro Induces Behavioral Changes In Sensory Neurons In Vitro B. Kulengowski, C. M. Calulot, J. A. Beller, T. M. Hering, and D. M. Snow B. Kulengowski, C. M. Calulot, J. A. Beller, T. M. Hering, and D. M. Snow B. Kulengowski, C. M. Calulot, J. A. Beller, T. M. Hering, and D. M. Snow

P-87 Meningeal/Fibrotic Scar Removal In Axolotl Spinal Cord Regeneration P-87 Meningeal/Fibrotic Scar Removal In Axolotl Spinal Cord Regeneration P-87 Meningeal/Fibrotic Scar Removal In Axolotl Spinal Cord Regeneration D.A. Sarria, H.V. Nguyen, M.W. Egar and E.A.G. Chernoff D.A. Sarria, H.V. Nguyen, M.W. Egar and E.A.G. Chernoff D.A. Sarria, H.V. Nguyen, M.W. Egar and E.A.G. Chernoff

P-88 Age and Time Since Injury Are Associated With Larger Cortical Activation P-88 Age and Time Since Injury Are Associated With Larger Cortical Activation P-88 Age and Time Since Injury Are Associated With Larger Cortical Activation After Incomplete Spinal Cord Injury After Incomplete Spinal Cord Injury After Incomplete Spinal Cord Injury S. C. Cramer, S. Kim, R. Gramer, S. Page, K. G. Sharp S. C. Cramer, S. Kim, R. Gramer, S. Page, K. G. Sharp S. C. Cramer, S. Kim, R. Gramer, S. Page, K. G. Sharp

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 33 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 33 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 33 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

P-1 Impaired Degeneration And expression related to axon guidance and P-1 Impaired Degeneration And expression related to axon guidance and P-1 Impaired Degeneration And expression related to axon guidance and Regeneration Of Peripheral Motor Axons Of neuroinflammation. At 7 days after lesion we Regeneration Of Peripheral Motor Axons Of neuroinflammation. At 7 days after lesion we Regeneration Of Peripheral Motor Axons Of neuroinflammation. At 7 days after lesion we Mice Heterozygously Deficient For The found that on the lesioned side, a series of genes Mice Heterozygously Deficient For The found that on the lesioned side, a series of genes Mice Heterozygously Deficient For The found that on the lesioned side, a series of genes Myelin Protein P0 Gene (Dnm3, Paxip1, Aspa, Tmod1, Frzb, Slitrk6, Myelin Protein P0 Gene (Dnm3, Paxip1, Aspa, Tmod1, Frzb, Slitrk6, Myelin Protein P0 Gene (Dnm3, Paxip1, Aspa, Tmod1, Frzb, Slitrk6, Thy1, Met, Sytl2, Sema3e, Fbn2, Akap6, Thy1, Met, Sytl2, Sema3e, Fbn2, Akap6, Thy1, Met, Sytl2, Sema3e, Fbn2, Akap6, M. Moldovan1, M. Rosberg1, J. Vikeså2, F. C. Snord52 and Gnb4) were up-regulated less in M. Moldovan1, M. Rosberg1, J. Vikeså2, F. C. Snord52 and Gnb4) were up-regulated less in M. Moldovan1, M. Rosberg1, J. Vikeså2, F. C. Snord52 and Gnb4) were up-regulated less in 2 1,3 2 1,3 2 1,3 Nielsen , C. Krarup P0+/- as compared to WT, whereas on the Nielsen , C. Krarup P0+/- as compared to WT, whereas on the Nielsen , C. Krarup P0+/- as compared to WT, whereas on the 1Institute of Neuroscience and unlesioned side the expression of these genes 1Institute of Neuroscience and unlesioned side the expression of these genes 1Institute of Neuroscience and unlesioned side the expression of these genes Pharmacology, Panum, Copenhagen University, did not differ. CMAP recovery during Pharmacology, Panum, Copenhagen University, did not differ. CMAP recovery during Pharmacology, Panum, Copenhagen University, did not differ. CMAP recovery during 2 2 2 DK; Depatment of Clinical Biochemistry, regeneration appeared delayed in P0+/-, in DK; Depatment of Clinical Biochemistry, regeneration appeared delayed in P0+/-, in DK; Depatment of Clinical Biochemistry, regeneration appeared delayed in P0+/-, in Rigshospitalet, DK; 3Clinical Neurophysiology, agreement with reduced excitability and poor Rigshospitalet, DK; 3Clinical Neurophysiology, agreement with reduced excitability and poor Rigshospitalet, DK; 3Clinical Neurophysiology, agreement with reduced excitability and poor Rigshositalet, DK performance at Rotor-Rod after one month. Rigshositalet, DK performance at Rotor-Rod after one month. Rigshositalet, DK performance at Rotor-Rod after one month. Together, these data suggest that both axonal Together, these data suggest that both axonal Together, these data suggest that both axonal Mice with a heterozyogous knock-out of degeneration and regeneration are impaired in Mice with a heterozyogous knock-out of degeneration and regeneration are impaired in Mice with a heterozyogous knock-out of degeneration and regeneration are impaired in the myelin protein P0 gene (P0+/-) are models of the presence of mutant Schwann cells the myelin protein P0 gene (P0+/-) are models of the presence of mutant Schwann cells the myelin protein P0 gene (P0+/-) are models of the presence of mutant Schwann cells Charcot-Marie-Tooth disease. The mice are heterozygously deficient in the P0 gene. Charcot-Marie-Tooth disease. The mice are heterozygously deficient in the P0 gene. Charcot-Marie-Tooth disease. The mice are heterozygously deficient in the P0 gene. indistinguishable from wild-types (WT) at birth; indistinguishable from wild-types (WT) at birth; indistinguishable from wild-types (WT) at birth; however, from about 7 months of age, they P-2 Does The Canonical Wound Healing however, from about 7 months of age, they P-2 Does The Canonical Wound Healing however, from about 7 months of age, they P-2 Does The Canonical Wound Healing develop a slowly progressing demyelinating Model Help To Explain The Pathogenesis Of develop a slowly progressing demyelinating Model Help To Explain The Pathogenesis Of develop a slowly progressing demyelinating Model Help To Explain The Pathogenesis Of neuropathy. Although conduction slowing is Compression Neuropathies? neuropathy. Although conduction slowing is Compression Neuropathies? neuropathy. Although conduction slowing is Compression Neuropathies? known to be associated with a reduction of known to be associated with a reduction of known to be associated with a reduction of compound muscle action potential (CMAP) M. Lin; P. Hahn; J. Kang; D. Frump; J. Jung; compound muscle action potential (CMAP) M. Lin; P. Hahn; J. Kang; D. Frump; J. Jung; compound muscle action potential (CMAP) M. Lin; P. Hahn; J. Kang; D. Frump; J. Jung; amplitude, the relationship between T. Chao; R. Gupta amplitude, the relationship between T. Chao; R. Gupta amplitude, the relationship between T. Chao; R. Gupta demyelination and axonal loss remains poorly University of California, Irvine, Irvine, demyelination and axonal loss remains poorly University of California, Irvine, Irvine, demyelination and axonal loss remains poorly University of California, Irvine, Irvine, understood. CA understood. CA understood. CA The aim of this study was to compare The aim of this study was to compare The aim of this study was to compare degeneration and regeneration of peripheral Chronic nerve compression (CNC) degeneration and regeneration of peripheral Chronic nerve compression (CNC) degeneration and regeneration of peripheral Chronic nerve compression (CNC) motor axons in early symptomatic P0+/- and age injuries such as carpal tunnel syndrome cause motor axons in early symptomatic P0+/- and age injuries such as carpal tunnel syndrome cause motor axons in early symptomatic P0+/- and age injuries such as carpal tunnel syndrome cause matched WT. patients significant morbidity with the ensuing matched WT. patients significant morbidity with the ensuing matched WT. patients significant morbidity with the ensuing Right sciatic nerves were lesioned at the loss of sensation and motor function. Previous Right sciatic nerves were lesioned at the loss of sensation and motor function. Previous Right sciatic nerves were lesioned at the loss of sensation and motor function. Previous thigh. Changes of the tibial nerve at ankle were studies have demonstrated changes in Schwann thigh. Changes of the tibial nerve at ankle were studies have demonstrated changes in Schwann thigh. Changes of the tibial nerve at ankle were studies have demonstrated changes in Schwann investigated by electrophysiological, cell form and function with limited early axonal investigated by electrophysiological, cell form and function with limited early axonal investigated by electrophysiological, cell form and function with limited early axonal histological and molecular methods. In vivo pathology during the progression of CNC histological and molecular methods. In vivo pathology during the progression of CNC histological and molecular methods. In vivo pathology during the progression of CNC motor nerve electrophysiology was carried out injury. Recent advancements from our group motor nerve electrophysiology was carried out injury. Recent advancements from our group motor nerve electrophysiology was carried out injury. Recent advancements from our group by conventional conduction studies and axon have prompted a reinterpretation of compressive by conventional conduction studies and axon have prompted a reinterpretation of compressive by conventional conduction studies and axon have prompted a reinterpretation of compressive excitability studies using threshold tracking. The neuropathies as being an example of a wound- excitability studies using threshold tracking. The neuropathies as being an example of a wound- excitability studies using threshold tracking. The neuropathies as being an example of a wound- overall motor performance was investigated healing model with the associated phases of overall motor performance was investigated healing model with the associated phases of overall motor performance was investigated healing model with the associated phases of using Rotor-Rod. To map differences in inflammation, angiogenesis, cellular using Rotor-Rod. To map differences in inflammation, angiogenesis, cellular using Rotor-Rod. To map differences in inflammation, angiogenesis, cellular degeneration, we compared gene expression proliferation, and connective tissue remodeling. degeneration, we compared gene expression proliferation, and connective tissue remodeling. degeneration, we compared gene expression proliferation, and connective tissue remodeling. profiles in the distal stump of degenerated Here we demonstrate CNC injury induces a profiles in the distal stump of degenerated Here we demonstrate CNC injury induces a profiles in the distal stump of degenerated Here we demonstrate CNC injury induces a nerves using Affymetrix genechips. To evaluate progressive and significant increase in ECM nerves using Affymetrix genechips. To evaluate progressive and significant increase in ECM nerves using Affymetrix genechips. To evaluate progressive and significant increase in ECM regeneration we monitored the recovery of components including fibronectin, laminin, and regeneration we monitored the recovery of components including fibronectin, laminin, and regeneration we monitored the recovery of components including fibronectin, laminin, and motor function after crush, and then compared collagen type IV at the level of mRNA motor function after crush, and then compared collagen type IV at the level of mRNA motor function after crush, and then compared collagen type IV at the level of mRNA the fiber distribution by histology. transcription and protein translation. the fiber distribution by histology. transcription and protein translation. the fiber distribution by histology. transcription and protein translation. In both P0+/- and WT axonal Furthermore, we were able to localize their up- In both P0+/- and WT axonal Furthermore, we were able to localize their up- In both P0+/- and WT axonal Furthermore, we were able to localize their up- degeneration triggered a change of gene regulation to the site of CNC injury relative to degeneration triggered a change of gene regulation to the site of CNC injury relative to degeneration triggered a change of gene regulation to the site of CNC injury relative to controls supporting the hypothesis that CNC controls supporting the hypothesis that CNC controls supporting the hypothesis that CNC

34 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 34 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 34 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE injury does induce ECM remodeling. At later Soluble C3156-181 was applied into a sciatic nerve injury does induce ECM remodeling. At later Soluble C3156-181 was applied into a sciatic nerve injury does induce ECM remodeling. At later Soluble C3156-181 was applied into a sciatic nerve time points when the neural scar is well crush injury or the epineurial sutures after nerve time points when the neural scar is well crush injury or the epineurial sutures after nerve time points when the neural scar is well crush injury or the epineurial sutures after nerve established, functional assessment of time- autotransplantation. Here, we analysed the established, functional assessment of time- autotransplantation. Here, we analysed the established, functional assessment of time- autotransplantation. Here, we analysed the integrated blood flow dynamics using laser effects of C3156-181 on PNR through a 10 mm integrated blood flow dynamics using laser effects of C3156-181 on PNR through a 10 mm integrated blood flow dynamics using laser effects of C3156-181 on PNR through a 10 mm speckle imaging technology demonstrates epineurial pouch filled with PuraMatrixTM speckle imaging technology demonstrates epineurial pouch filled with PuraMatrixTM speckle imaging technology demonstrates epineurial pouch filled with PuraMatrixTM significant reduction of neurovascular flow at hydrogel containing 8 nmol C3156-181/kg. significant reduction of neurovascular flow at hydrogel containing 8 nmol C3156-181/kg. significant reduction of neurovascular flow at hydrogel containing 8 nmol C3156-181/kg. the site of compression. Current experiments Regarding the previous positive results, we the site of compression. Current experiments Regarding the previous positive results, we the site of compression. Current experiments Regarding the previous positive results, we with alpha-2 laminin deficient and Desert hypothesized that sustained release and thus with alpha-2 laminin deficient and Desert hypothesized that sustained release and thus with alpha-2 laminin deficient and Desert hypothesized that sustained release and thus hedgehog knockout mice will further elucidate prolonged presence of the C3156-181 would hedgehog knockout mice will further elucidate prolonged presence of the C3156-181 would hedgehog knockout mice will further elucidate prolonged presence of the C3156-181 would the role of fibroblasts and Schwann cells within increase axonal and functional regeneration in the role of fibroblasts and Schwann cells within increase axonal and functional regeneration in the role of fibroblasts and Schwann cells within increase axonal and functional regeneration in the basal lamina of the ECM following CNC comparison to application of phosphate buffered the basal lamina of the ECM following CNC comparison to application of phosphate buffered the basal lamina of the ECM following CNC comparison to application of phosphate buffered injury. By considering the pattern of ECM saline (PBS) or C3bot in PuraMatrix. 10 mm injury. By considering the pattern of ECM saline (PBS) or C3bot in PuraMatrix. 10 mm injury. By considering the pattern of ECM saline (PBS) or C3bot in PuraMatrix. 10 mm expression with our quantitative and qualitative nerve autotransplantation served as positive expression with our quantitative and qualitative nerve autotransplantation served as positive expression with our quantitative and qualitative nerve autotransplantation served as positive findings in two different animal models, the data control (left sciatic nerves of adult rats; findings in two different animal models, the data control (left sciatic nerves of adult rats; findings in two different animal models, the data control (left sciatic nerves of adult rats; supports that CNC injury induces a biologic n=7/group). supports that CNC injury induces a biologic n=7/group). supports that CNC injury induces a biologic n=7/group). response which mimics canonical wound The 10 mm epineurial pouch was response which mimics canonical wound The 10 mm epineurial pouch was response which mimics canonical wound The 10 mm epineurial pouch was healing and leads to up-regulation of ECM prepared by stripping-off nerve fascicles healing and leads to up-regulation of ECM prepared by stripping-off nerve fascicles healing and leads to up-regulation of ECM prepared by stripping-off nerve fascicles components with eventual scar formation. This through two epineurial windows. PuraMatrix components with eventual scar formation. This through two epineurial windows. PuraMatrix components with eventual scar formation. This through two epineurial windows. PuraMatrix pathway promotes tissue repair by modifying formulations were then injected as replacement. pathway promotes tissue repair by modifying formulations were then injected as replacement. pathway promotes tissue repair by modifying formulations were then injected as replacement. structural support of the peripheral nerve after During 12 post operational weeks, we structural support of the peripheral nerve after During 12 post operational weeks, we structural support of the peripheral nerve after During 12 post operational weeks, we CNC injury and thereby restricts the capacity performed functional tests; weekly: Static CNC injury and thereby restricts the capacity performed functional tests; weekly: Static CNC injury and thereby restricts the capacity performed functional tests; weekly: Static for functional tissue and nerve regeneration with Sciatic Index (SSI)-Evaluation (motor task), for functional tissue and nerve regeneration with Sciatic Index (SSI)-Evaluation (motor task), for functional tissue and nerve regeneration with Sciatic Index (SSI)-Evaluation (motor task), surgical management alone after this Pinch-Test (mechanosensitivity), bi-weekly: surgical management alone after this Pinch-Test (mechanosensitivity), bi-weekly: surgical management alone after this Pinch-Test (mechanosensitivity), bi-weekly: remodeling has occurred. As such, this work non-invasive electrodiagnostic measurements remodeling has occurred. As such, this work non-invasive electrodiagnostic measurements remodeling has occurred. As such, this work non-invasive electrodiagnostic measurements provides the basis for the development of (motor function). By end of the observation provides the basis for the development of (motor function). By end of the observation provides the basis for the development of (motor function). By end of the observation adjuvant treatment to improve functional period, invasive electrodiagnostic adjuvant treatment to improve functional period, invasive electrodiagnostic adjuvant treatment to improve functional period, invasive electrodiagnostic recovery for compression neuropathies. measurements, lower limb muscle weight recovery for compression neuropathies. measurements, lower limb muscle weight recovery for compression neuropathies. measurements, lower limb muscle weight analysis and histomorphometrical analysis was analysis and histomorphometrical analysis was analysis and histomorphometrical analysis was P-3 Efficacy Of C3 Peptide To Promote performed. P-3 Efficacy Of C3 Peptide To Promote performed. P-3 Efficacy Of C3 Peptide To Promote performed. Peripheral Nerve Regeneration Depends On Preliminary data demonstrate that Peripheral Nerve Regeneration Depends On Preliminary data demonstrate that Peripheral Nerve Regeneration Depends On Preliminary data demonstrate that The Mode Of Application. autotransplantation is still the superior The Mode Of Application. autotransplantation is still the superior The Mode Of Application. autotransplantation is still the superior condition. SSI-evaluation did not show any condition. SSI-evaluation did not show any condition. SSI-evaluation did not show any K. Haastert-Talini1,2, T. Hettwer1, A. Rohrbeck3, significant recovery in presence of C3bot and K. Haastert-Talini1,2, T. Hettwer1, A. Rohrbeck3, significant recovery in presence of C3bot and K. Haastert-Talini1,2, T. Hettwer1, A. Rohrbeck3, significant recovery in presence of C3bot and I. Just3, C. Grothe1,2 C3156-181. Recovery of mechanosensitivity and I. Just3, C. Grothe1,2 C3156-181. Recovery of mechanosensitivity and I. Just3, C. Grothe1,2 C3156-181. Recovery of mechanosensitivity and 1Hannover Medical School, Institute of functional axons (non-invasive 1Hannover Medical School, Institute of functional axons (non-invasive 1Hannover Medical School, Institute of functional axons (non-invasive Neuroanatomy, Hannover, Germany, 2Center electrodiagnostics) in the C3156-181 group only Neuroanatomy, Hannover, Germany, 2Center electrodiagnostics) in the C3156-181 group only Neuroanatomy, Hannover, Germany, 2Center electrodiagnostics) in the C3156-181 group only for Systems Neurosciences (ZSN) Hannover, slightly precedes the PBS and C3bot groups. for Systems Neurosciences (ZSN) Hannover, slightly precedes the PBS and C3bot groups. for Systems Neurosciences (ZSN) Hannover, slightly precedes the PBS and C3bot groups. Germany and 3Hannover Medical School, The lower limb muscle weight did recover to the Germany and 3Hannover Medical School, The lower limb muscle weight did recover to the Germany and 3Hannover Medical School, The lower limb muscle weight did recover to the Institute of Toxicology, Hannover, Germany lowest level in the C3156-181. Institute of Toxicology, Hannover, Germany lowest level in the C3156-181. Institute of Toxicology, Hannover, Germany lowest level in the C3156-181. In the previous study (Huelsenbeck et al, In the previous study (Huelsenbeck et al, In the previous study (Huelsenbeck et al, We have recently shown that one-time Neurotherapeutics 2011), effects of C3156-181 We have recently shown that one-time Neurotherapeutics 2011), effects of C3156-181 We have recently shown that one-time Neurotherapeutics 2011), effects of C3156-181 administration of C3156-181 peptide derived from were significantly stronger than those of C3bot administration of C3156-181 peptide derived from were significantly stronger than those of C3bot administration of C3156-181 peptide derived from were significantly stronger than those of C3bot the Rho-inactivating C3 transferase (C3bot) or vehicle only, while here both groups show the Rho-inactivating C3 transferase (C3bot) or vehicle only, while here both groups show the Rho-inactivating C3 transferase (C3bot) or vehicle only, while here both groups show from Clostridium botulinum, promotes less regeneration than under control conditions. from Clostridium botulinum, promotes less regeneration than under control conditions. from Clostridium botulinum, promotes less regeneration than under control conditions. peripheral nerve regeneration (PNR) Further data analysis will demonstrate if indeed, peripheral nerve regeneration (PNR) Further data analysis will demonstrate if indeed, peripheral nerve regeneration (PNR) Further data analysis will demonstrate if indeed, (Huelsenbeck et al, Neurotherapeutics 2011). prolonged availability of C3156-181 at the lesion (Huelsenbeck et al, Neurotherapeutics 2011). prolonged availability of C3156-181 at the lesion (Huelsenbeck et al, Neurotherapeutics 2011). prolonged availability of C3156-181 at the lesion

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 35 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 35 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 35 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE site impairs PNR in contrast to the one-time regeneration was seen across a 10 mm nerve site impairs PNR in contrast to the one-time regeneration was seen across a 10 mm nerve site impairs PNR in contrast to the one-time regeneration was seen across a 10 mm nerve administration. gap. Initial histological results showed similar administration. gap. Initial histological results showed similar administration. gap. Initial histological results showed similar levels of regeneration to that of a hollow levels of regeneration to that of a hollow levels of regeneration to that of a hollow P-4 Peripheral Nerve Repair: An In Vivo conduit. However retrograde tracing results P-4 Peripheral Nerve Repair: An In Vivo conduit. However retrograde tracing results P-4 Peripheral Nerve Repair: An In Vivo conduit. However retrograde tracing results Investigation of Structurally Enhanced Nerve showed a significant increase in targeted nerve Investigation of Structurally Enhanced Nerve showed a significant increase in targeted nerve Investigation of Structurally Enhanced Nerve showed a significant increase in targeted nerve Guidance Conduits regeneration in all EGF groups versus the Guidance Conduits regeneration in all EGF groups versus the Guidance Conduits regeneration in all EGF groups versus the autograft group. In conclusion: EGFs show the autograft group. In conclusion: EGFs show the autograft group. In conclusion: EGFs show the W. Daly 1, M. Abu-Rub 1, B. Breen 1, D. ability, in vitro, to increase aligned nerve W. Daly 1, M. Abu-Rub 1, B. Breen 1, D. ability, in vitro, to increase aligned nerve W. Daly 1, M. Abu-Rub 1, B. Breen 1, D. ability, in vitro, to increase aligned nerve Zeugolis 1, C.O’Connell2, L. Yao1, growth. In vivo, the addition of EGFS, did not Zeugolis 1, C.O’Connell2, L. Yao1, growth. In vivo, the addition of EGFS, did not Zeugolis 1, C.O’Connell2, L. Yao1, growth. In vivo, the addition of EGFS, did not A. Windebank3, A. Pandit1 significantly affect the level of nerve A. Windebank3, A. Pandit1 significantly affect the level of nerve A. Windebank3, A. Pandit1 significantly affect the level of nerve 1Network of Excellence for Functional regeneration but the addition of EGFS within 1Network of Excellence for Functional regeneration but the addition of EGFS within 1Network of Excellence for Functional regeneration but the addition of EGFS within Biomaterials, 2 National Centre for Laser the conduit showed a significant increase in Biomaterials, 2 National Centre for Laser the conduit showed a significant increase in Biomaterials, 2 National Centre for Laser the conduit showed a significant increase in Applications, National University of Ireland, targeted nerve regeneration. This targeted nerve Applications, National University of Ireland, targeted nerve regeneration. This targeted nerve Applications, National University of Ireland, targeted nerve regeneration. This targeted nerve Galway, Ireland 3 Cellular Neurobiology regeneration is a critical step to improve current Galway, Ireland 3 Cellular Neurobiology regeneration is a critical step to improve current Galway, Ireland 3 Cellular Neurobiology regeneration is a critical step to improve current Laboratory, Mayo Clinic, Rochester, Minnesota, NGCs. Laboratory, Mayo Clinic, Rochester, Minnesota, NGCs. Laboratory, Mayo Clinic, Rochester, Minnesota, NGCs. USA USA USA P-5 Mmp-3 Inhibition Blocks Degradation P-5 Mmp-3 Inhibition Blocks Degradation P-5 Mmp-3 Inhibition Blocks Degradation This study investigates the use of of The Neuromuscular Junction After This study investigates the use of of The Neuromuscular Junction After This study investigates the use of of The Neuromuscular Junction After extruded collagen fibres (EGFs) as an Traumatic Peripheral Nerve Injury extruded collagen fibres (EGFs) as an Traumatic Peripheral Nerve Injury extruded collagen fibres (EGFs) as an Traumatic Peripheral Nerve Injury intraluminal filler, to improve existing nerve intraluminal filler, to improve existing nerve intraluminal filler, to improve existing nerve guidance conduits (NGCs). It is hypothesized T. Chao; D. Frump; N. Nassiri; J. Jung; P. guidance conduits (NGCs). It is hypothesized T. Chao; D. Frump; N. Nassiri; J. Jung; P. guidance conduits (NGCs). It is hypothesized T. Chao; D. Frump; N. Nassiri; J. Jung; P. that EGFs increase the surface area available for Hahn; T. Mozaffar; R. Gupta that EGFs increase the surface area available for Hahn; T. Mozaffar; R. Gupta that EGFs increase the surface area available for Hahn; T. Mozaffar; R. Gupta cell adhesion, enhancing cell migration, and University Of California, Irvine, CA cell adhesion, enhancing cell migration, and University Of California, Irvine, CA cell adhesion, enhancing cell migration, and University Of California, Irvine, CA providing topographical guidance cues for providing topographical guidance cues for providing topographical guidance cues for regenerating axons. This study involves the Traumatic peripheral nerve injuries often regenerating axons. This study involves the Traumatic peripheral nerve injuries often regenerating axons. This study involves the Traumatic peripheral nerve injuries often characterisation of the EGFs in vitro and in produce significant functional deficits despite characterisation of the EGFs in vitro and in produce significant functional deficits despite characterisation of the EGFs in vitro and in produce significant functional deficits despite vivo as a platform for cell migration and optimal medical management. The loss of vivo as a platform for cell migration and optimal medical management. The loss of vivo as a platform for cell migration and optimal medical management. The loss of topographical guidance of axons. The EGFs targets for reinnervation leads to a down- topographical guidance of axons. The EGFs targets for reinnervation leads to a down- topographical guidance of axons. The EGFs targets for reinnervation leads to a down- were fabricated in a multi-step process. EGF regulation of trophic factors guiding were fabricated in a multi-step process. EGF regulation of trophic factors guiding were fabricated in a multi-step process. EGF regulation of trophic factors guiding structure was analysed using standard surface regenerating axons with the subsequent end- structure was analysed using standard surface regenerating axons with the subsequent end- structure was analysed using standard surface regenerating axons with the subsequent end- characterisation techniques. Neuronal organ atrophy of the neuromuscular junction characterisation techniques. Neuronal organ atrophy of the neuromuscular junction characterisation techniques. Neuronal organ atrophy of the neuromuscular junction interaction and cell migration, on the EGFs, was (NMJ). It is known that NMJ assembly and interaction and cell migration, on the EGFs, was (NMJ). It is known that NMJ assembly and interaction and cell migration, on the EGFs, was (NMJ). It is known that NMJ assembly and assessed using rat PC12 cells and 3T3 fibroblast maintenance depends highly on the interaction assessed using rat PC12 cells and 3T3 fibroblast maintenance depends highly on the interaction assessed using rat PC12 cells and 3T3 fibroblast maintenance depends highly on the interaction cells respectively. between agrin and its receptor, muscle- specific cells respectively. between agrin and its receptor, muscle- specific cells respectively. between agrin and its receptor, muscle- specific Following in vitro characterization, 18 EGFs kinase (MuSK). The NMJ matures during Following in vitro characterization, 18 EGFs kinase (MuSK). The NMJ matures during Following in vitro characterization, 18 EGFs kinase (MuSK). The NMJ matures during were enclosed within a collagen NGC, and development under the direction of signaling were enclosed within a collagen NGC, and development under the direction of signaling were enclosed within a collagen NGC, and development under the direction of signaling implanted in a rat sciatic nerve model for 16 mechanisms initiated with binding of agrin to implanted in a rat sciatic nerve model for 16 mechanisms initiated with binding of agrin to implanted in a rat sciatic nerve model for 16 mechanisms initiated with binding of agrin to weeks. 16 weeks post implantation, MuSK. Agrin is degraded by matrix weeks. 16 weeks post implantation, MuSK. Agrin is degraded by matrix weeks. 16 weeks post implantation, MuSK. Agrin is degraded by matrix simultaneous retrograde tracing and nerve metalloproteinase 3 (MMP-3)produced by the simultaneous retrograde tracing and nerve metalloproteinase 3 (MMP-3)produced by the simultaneous retrograde tracing and nerve metalloproteinase 3 (MMP-3)produced by the morphometry analyses were carried out. In perisynaptic Schwann cell. The current study morphometry analyses were carried out. In perisynaptic Schwann cell. The current study morphometry analyses were carried out. In perisynaptic Schwann cell. The current study vitro assessment of the neural interaction, of the focuses on assessing the NMJ after long-term vitro assessment of the neural interaction, of the focuses on assessing the NMJ after long-term vitro assessment of the neural interaction, of the focuses on assessing the NMJ after long-term EGFs, showed a significant increase in neurite denervation injury to simulate the clinical EGFs, showed a significant increase in neurite denervation injury to simulate the clinical EGFs, showed a significant increase in neurite denervation injury to simulate the clinical length and higher alignment versus control scenario. Specimens from both wild-type and length and higher alignment versus control scenario. Specimens from both wild-type and length and higher alignment versus control scenario. Specimens from both wild-type and collagen fibres (n=3, p<0.05) and 3T3 cells MMP-3 knockout mice were harvested at 3 collagen fibres (n=3, p<0.05) and 3T3 cells MMP-3 knockout mice were harvested at 3 collagen fibres (n=3, p<0.05) and 3T3 cells MMP-3 knockout mice were harvested at 3 successfully migrating across the fibres. 16 days, 7 days, 14 days, 1 month, 4 months (n=4 successfully migrating across the fibres. 16 days, 7 days, 14 days, 1 month, 4 months (n=4 successfully migrating across the fibres. 16 days, 7 days, 14 days, 1 month, 4 months (n=4 weeks post implantation, successful nerve all time points) post-injury. Immuno- weeks post implantation, successful nerve all time points) post-injury. Immuno- weeks post implantation, successful nerve all time points) post-injury. Immuno-

36 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 36 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 36 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE histochemical analysis was performed to define because of the loss of ascending transmission, histochemical analysis was performed to define because of the loss of ascending transmission, histochemical analysis was performed to define because of the loss of ascending transmission, the integrity of all three components of the NMJ but this does not prevent the effects on sensory the integrity of all three components of the NMJ but this does not prevent the effects on sensory the integrity of all three components of the NMJ but this does not prevent the effects on sensory after denervation. Agrin levels were quantified and spinal neurons and spinal circuitry. Further, after denervation. Agrin levels were quantified and spinal neurons and spinal circuitry. Further, after denervation. Agrin levels were quantified and spinal neurons and spinal circuitry. Further, to determine if destabilization of the NMJ because SCI often includes loss of descending to determine if destabilization of the NMJ because SCI often includes loss of descending to determine if destabilization of the NMJ because SCI often includes loss of descending corresponds to a decrease in agrin. Specimens pain modulation, the effects of tissue injury on corresponds to a decrease in agrin. Specimens pain modulation, the effects of tissue injury on corresponds to a decrease in agrin. Specimens pain modulation, the effects of tissue injury on from normal muscle contained Ach receptors the nervous system may be worse than in the from normal muscle contained Ach receptors the nervous system may be worse than in the from normal muscle contained Ach receptors the nervous system may be worse than in the with round profiles and multiple perforations spinal-intact condition, but occur subliminally with round profiles and multiple perforations spinal-intact condition, but occur subliminally with round profiles and multiple perforations spinal-intact condition, but occur subliminally consistent with the normal phenotype. In (clinically and experimentally). consistent with the normal phenotype. In (clinically and experimentally). consistent with the normal phenotype. In (clinically and experimentally). contrast, denervated muscles demonstrated We recently discovered that damage to contrast, denervated muscles demonstrated We recently discovered that damage to contrast, denervated muscles demonstrated We recently discovered that damage to significant attenuation of Ach receptor profiles. peripheral tissues leads to many of the same significant attenuation of Ach receptor profiles. peripheral tissues leads to many of the same significant attenuation of Ach receptor profiles. peripheral tissues leads to many of the same Surprisingly, denervated muscles from MMP-3 responses in dorsal root ganglion (DRG) Surprisingly, denervated muscles from MMP-3 responses in dorsal root ganglion (DRG) Surprisingly, denervated muscles from MMP-3 responses in dorsal root ganglion (DRG) animals contained receptor profiles with areas sensory neurons innervating that tissue as occur animals contained receptor profiles with areas sensory neurons innervating that tissue as occur animals contained receptor profiles with areas sensory neurons innervating that tissue as occur greater than contralateral specimens. Western with direct injury to a peripheral nerve. There greater than contralateral specimens. Western with direct injury to a peripheral nerve. There greater than contralateral specimens. Western with direct injury to a peripheral nerve. There blot data confirmed a decrease in agrin after was strong and sustained expression of genes blot data confirmed a decrease in agrin after was strong and sustained expression of genes blot data confirmed a decrease in agrin after was strong and sustained expression of genes denervation in wildtype mice. Conversely, agrin related to axonal regeneration. Injury of denervation in wildtype mice. Conversely, agrin related to axonal regeneration. Injury of denervation in wildtype mice. Conversely, agrin related to axonal regeneration. Injury of isoforms were upregulated following peripheral nerves is a standard method for isoforms were upregulated following peripheral nerves is a standard method for isoforms were upregulated following peripheral nerves is a standard method for denervation in MMP3 knockout mice. The inducing axonal growth in the injured spinal denervation in MMP3 knockout mice. The inducing axonal growth in the injured spinal denervation in MMP3 knockout mice. The inducing axonal growth in the injured spinal ability of the Ach receptor to resist cord, and the process exhibits a conditioning ability of the Ach receptor to resist cord, and the process exhibits a conditioning ability of the Ach receptor to resist cord, and the process exhibits a conditioning destabilization after prolonged denervation response (i.e., growth after 2nd injury is greater destabilization after prolonged denervation response (i.e., growth after 2nd injury is greater destabilization after prolonged denervation response (i.e., growth after 2nd injury is greater secondary to the elimination of MMP-3 and the than after single). Accordingly, the response of secondary to the elimination of MMP-3 and the than after single). Accordingly, the response of secondary to the elimination of MMP-3 and the than after single). Accordingly, the response of ensuing persistence of agrin at the NMJ DRG to repeated tissue damage was ensuing persistence of agrin at the NMJ DRG to repeated tissue damage was ensuing persistence of agrin at the NMJ DRG to repeated tissue damage was provides an exciting novel opportunity to synergistically-enhanced over the response to provides an exciting novel opportunity to synergistically-enhanced over the response to provides an exciting novel opportunity to synergistically-enhanced over the response to improve functional outcomes after traumatic single tissue damage not only for regeneration- improve functional outcomes after traumatic single tissue damage not only for regeneration- improve functional outcomes after traumatic single tissue damage not only for regeneration- nerve injuries. related genes, but also those linked to chronic nerve injuries. related genes, but also those linked to chronic nerve injuries. related genes, but also those linked to chronic pain. Repeated tissue damage induced changes pain. Repeated tissue damage induced changes pain. Repeated tissue damage induced changes P-6 Sensory Neuron Responses to in DRG that mimicked those induced by nerve- P-6 Sensory Neuron Responses to in DRG that mimicked those induced by nerve- P-6 Sensory Neuron Responses to in DRG that mimicked those induced by nerve- Peripheral Tissue-Damage: Implications for injury models of chronic pain, whereas a single Peripheral Tissue-Damage: Implications for injury models of chronic pain, whereas a single Peripheral Tissue-Damage: Implications for injury models of chronic pain, whereas a single SCI Secondary Conditions bout of tissue damage had little effect. SCI Secondary Conditions bout of tissue damage had little effect. SCI Secondary Conditions bout of tissue damage had little effect. These findings may have implications These findings may have implications These findings may have implications J.C. Petruska1,2, C.H. Hill3,4, K.K. Rau1,2 for the consequences of post-SCI conditions and J.C. Petruska1,2, C.H. Hill3,4, K.K. Rau1,2 for the consequences of post-SCI conditions and J.C. Petruska1,2, C.H. Hill3,4, K.K. Rau1,2 for the consequences of post-SCI conditions and 1University of Louisville Departments of their treatment standards. For the research and 1University of Louisville Departments of their treatment standards. For the research and 1University of Louisville Departments of their treatment standards. For the research and Anatomical Sciences and Neurobiology, and clinical communities to develop and implement Anatomical Sciences and Neurobiology, and clinical communities to develop and implement Anatomical Sciences and Neurobiology, and clinical communities to develop and implement Neurological Surgery; 2Kentucky Spinal Cord effective therapies, particularly activity-based Neurological Surgery; 2Kentucky Spinal Cord effective therapies, particularly activity-based Neurological Surgery; 2Kentucky Spinal Cord effective therapies, particularly activity-based Injury Research Center, Louisville, KY; 3Burke therapies which rely on proper sensory input, it Injury Research Center, Louisville, KY; 3Burke therapies which rely on proper sensory input, it Injury Research Center, Louisville, KY; 3Burke therapies which rely on proper sensory input, it Medical Research Institute; 4Department of is important that the status of sensory neurons Medical Research Institute; 4Department of is important that the status of sensory neurons Medical Research Institute; 4Department of is important that the status of sensory neurons Neurology and Neuroscience, Weill Cornell and spinal circuitry below the level of the injury Neurology and Neuroscience, Weill Cornell and spinal circuitry below the level of the injury Neurology and Neuroscience, Weill Cornell and spinal circuitry below the level of the injury Medical College, White Plains, NY be addressed. Medical College, White Plains, NY be addressed. Medical College, White Plains, NY be addressed.

Spinal cord injured individuals P-7 Aspartate Aminotransferase Is Spinal cord injured individuals P-7 Aspartate Aminotransferase Is Spinal cord injured individuals P-7 Aspartate Aminotransferase Is frequently and repeatedly experience tissue Elevated In Rat Dorsal Root Ganglion frequently and repeatedly experience tissue Elevated In Rat Dorsal Root Ganglion frequently and repeatedly experience tissue Elevated In Rat Dorsal Root Ganglion damage secondary to the SCI itself (pressure Neurons During Regeneration Following damage secondary to the SCI itself (pressure Neurons During Regeneration Following damage secondary to the SCI itself (pressure Neurons During Regeneration Following ulcers, bowel impaction/colitis, lacerations, Sciatic Nerve Crush ulcers, bowel impaction/colitis, lacerations, Sciatic Nerve Crush ulcers, bowel impaction/colitis, lacerations, Sciatic Nerve Crush etc.). In spinal intact individuals such repeated etc.). In spinal intact individuals such repeated etc.). In spinal intact individuals such repeated tissue damage often leads to neuropathic pain. B. Bolt, Z. Zhang, S. Alothman, K.E. Miller tissue damage often leads to neuropathic pain. B. Bolt, Z. Zhang, S. Alothman, K.E. Miller tissue damage often leads to neuropathic pain. B. Bolt, Z. Zhang, S. Alothman, K.E. Miller In the SCI population, such conditions below In the SCI population, such conditions below In the SCI population, such conditions below the level of the injury may not lead to pain the level of the injury may not lead to pain the level of the injury may not lead to pain

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 37 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 37 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 37 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

Department of Anatomy and Cell determine if this also occurs in medium and Department of Anatomy and Cell determine if this also occurs in medium and Department of Anatomy and Cell determine if this also occurs in medium and Biology, Oklahoma State University Center for large sized neurons. Biology, Oklahoma State University Center for large sized neurons. Biology, Oklahoma State University Center for large sized neurons. Health Sciences, Tulsa, OK 74107 Sponsored by NIH AR047410 (KEM). Health Sciences, Tulsa, OK 74107 Sponsored by NIH AR047410 (KEM). Health Sciences, Tulsa, OK 74107 Sponsored by NIH AR047410 (KEM).

The sensory neurons of the dorsal root P-8 Vesicular Glutamate Transporter 2 The sensory neurons of the dorsal root P-8 Vesicular Glutamate Transporter 2 The sensory neurons of the dorsal root P-8 Vesicular Glutamate Transporter 2 ganglia (DRG) are glutamatergic, utilizing Expression Is Altered In Dorsal Root ganglia (DRG) are glutamatergic, utilizing Expression Is Altered In Dorsal Root ganglia (DRG) are glutamatergic, utilizing Expression Is Altered In Dorsal Root glutaminase (GLS) in the glutamine cycle for Ganglion Neurons During The Regenerative glutaminase (GLS) in the glutamine cycle for Ganglion Neurons During The Regenerative glutaminase (GLS) in the glutamine cycle for Ganglion Neurons During The Regenerative glutamate production (Miller et al., Pharmacol Phase Following Sciatic Nerve Crush. glutamate production (Miller et al., Pharmacol Phase Following Sciatic Nerve Crush. glutamate production (Miller et al., Pharmacol Phase Following Sciatic Nerve Crush. Ther 130:283–2011). Aspartate Ther 130:283–2011). Aspartate Ther 130:283–2011). Aspartate aminotransferase (AST) is a key enzyme linking S. Alothman, Z. Zhang, B. Bolt, K.E. Miller aminotransferase (AST) is a key enzyme linking S. Alothman, Z. Zhang, B. Bolt, K.E. Miller aminotransferase (AST) is a key enzyme linking S. Alothman, Z. Zhang, B. Bolt, K.E. Miller the neuronal TCA cycle with the glutamine Department of Anatomy and Cell the neuronal TCA cycle with the glutamine Department of Anatomy and Cell the neuronal TCA cycle with the glutamine Department of Anatomy and Cell cycle for synthesis of glutamate. We have Biology, Oklahoma State University Center for cycle for synthesis of glutamate. We have Biology, Oklahoma State University Center for cycle for synthesis of glutamate. We have Biology, Oklahoma State University Center for previously demonstrated that AST is expressed Health Sciences, Tulsa, OK 74107 previously demonstrated that AST is expressed Health Sciences, Tulsa, OK 74107 previously demonstrated that AST is expressed Health Sciences, Tulsa, OK 74107 in large (>800 µm2), medium (400-800 µm2) in large (>800 µm2), medium (400-800 µm2) in large (>800 µm2), medium (400-800 µm2) and small (100-400µm2) DRG neurons Dorsal root ganglion (DRG) neurons are and small (100-400µm2) DRG neurons Dorsal root ganglion (DRG) neurons are and small (100-400µm2) DRG neurons Dorsal root ganglion (DRG) neurons are corresponding to Aβ-, Aδ-, and C-fiber neurons, glutamatergic using glutamate as a corresponding to Aβ-, Aδ-, and C-fiber neurons, glutamatergic using glutamate as a corresponding to Aβ-, Aδ-, and C-fiber neurons, glutamatergic using glutamate as a respectively. During the acute phase of adjuvant neurotransmitter in the spinal cord and, in a respectively. During the acute phase of adjuvant neurotransmitter in the spinal cord and, in a respectively. During the acute phase of adjuvant neurotransmitter in the spinal cord and, in a induced arthritis, there is an increase in AST in subset of DRG neurons, releasing glutamate into induced arthritis, there is an increase in AST in subset of DRG neurons, releasing glutamate into induced arthritis, there is an increase in AST in subset of DRG neurons, releasing glutamate into small neurons in rat DRG. The fate of AST peripheral tissue (Miller et al., Pharmacol Ther small neurons in rat DRG. The fate of AST peripheral tissue (Miller et al., Pharmacol Ther small neurons in rat DRG. The fate of AST peripheral tissue (Miller et al., Pharmacol Ther expression in the regenerative phase following 130(3):283-309, 2011). DRG neurons express expression in the regenerative phase following 130(3):283-309, 2011). DRG neurons express expression in the regenerative phase following 130(3):283-309, 2011). DRG neurons express peripheral nerve injury is unknown. We either vesicular glutamate transporter (VGLUT) peripheral nerve injury is unknown. We either vesicular glutamate transporter (VGLUT) peripheral nerve injury is unknown. We either vesicular glutamate transporter (VGLUT) hypothesize that AST would be elevated in the 1 or 2 for the release of glutamate (Brumovsky hypothesize that AST would be elevated in the 1 or 2 for the release of glutamate (Brumovsky hypothesize that AST would be elevated in the 1 or 2 for the release of glutamate (Brumovsky DRG following sciatic nerve crush. In the et al., Neuroscience147(2):469-90, 2007). DRG following sciatic nerve crush. In the et al., Neuroscience147(2):469-90, 2007). DRG following sciatic nerve crush. In the et al., Neuroscience147(2):469-90, 2007). present study, we evaluated changes in AST Previous studies have suggested alterations in present study, we evaluated changes in AST Previous studies have suggested alterations in present study, we evaluated changes in AST Previous studies have suggested alterations in immunoreactivity in DRG neuronal cell bodies glutamate metabolism in DRG neurons in the immunoreactivity in DRG neuronal cell bodies glutamate metabolism in DRG neurons in the immunoreactivity in DRG neuronal cell bodies glutamate metabolism in DRG neurons in the at 14 days following sciatic nerve crush. Adult regenerative phase following peripheral nerve at 14 days following sciatic nerve crush. Adult regenerative phase following peripheral nerve at 14 days following sciatic nerve crush. Adult regenerative phase following peripheral nerve Sprague Dawley rats were anesthetized, the injury (Porcellati and Thompson, J Neurochem Sprague Dawley rats were anesthetized, the injury (Porcellati and Thompson, J Neurochem Sprague Dawley rats were anesthetized, the injury (Porcellati and Thompson, J Neurochem sciatic nerve was exposed mid-thigh, and the 1(4):340-7, 1957; Johnson, Experientia, sciatic nerve was exposed mid-thigh, and the 1(4):340-7, 1957; Johnson, Experientia, sciatic nerve was exposed mid-thigh, and the 1(4):340-7, 1957; Johnson, Experientia, nerve was crushed. Control rats received a skin 32(2):184-6, 1976), but it is unknown if there nerve was crushed. Control rats received a skin 32(2):184-6, 1976), but it is unknown if there nerve was crushed. Control rats received a skin 32(2):184-6, 1976), but it is unknown if there incision mid-thigh. After 14 days, rats were are changes in VGLUT expression. In the incision mid-thigh. After 14 days, rats were are changes in VGLUT expression. In the incision mid-thigh. After 14 days, rats were are changes in VGLUT expression. In the anesthetized and transcardially perfused with present study, we evaluated changes in anesthetized and transcardially perfused with present study, we evaluated changes in anesthetized and transcardially perfused with present study, we evaluated changes in fixative. L4 DRG’s were processed for AST VGLUT2 immunoreactivity in DRG neuronal fixative. L4 DRG’s were processed for AST VGLUT2 immunoreactivity in DRG neuronal fixative. L4 DRG’s were processed for AST VGLUT2 immunoreactivity in DRG neuronal immunohistochemistry. DRG sections were cell bodies at 14 days following sciatic nerve immunohistochemistry. DRG sections were cell bodies at 14 days following sciatic nerve immunohistochemistry. DRG sections were cell bodies at 14 days following sciatic nerve observed and photographed with Olympus BX5 crush. Adult Sprague Dawley rats were observed and photographed with Olympus BX5 crush. Adult Sprague Dawley rats were observed and photographed with Olympus BX5 crush. Adult Sprague Dawley rats were epifluorescence microscope and SPOT camera. anesthetized, the sciatic nerve was exposed mid- epifluorescence microscope and SPOT camera. anesthetized, the sciatic nerve was exposed mid- epifluorescence microscope and SPOT camera. anesthetized, the sciatic nerve was exposed mid- Image J (NIH) was used to evaluate AST thigh, and the nerve was crushed with a Image J (NIH) was used to evaluate AST thigh, and the nerve was crushed with a Image J (NIH) was used to evaluate AST thigh, and the nerve was crushed with a immunoreactive intensity. We observed a hemostat. Control rats received only a surgical immunoreactive intensity. We observed a hemostat. Control rats received only a surgical immunoreactive intensity. We observed a hemostat. Control rats received only a surgical qualitative elevation in AST expression in all incision. After 14 days, rats were anesthetized qualitative elevation in AST expression in all incision. After 14 days, rats were anesthetized qualitative elevation in AST expression in all incision. After 14 days, rats were anesthetized neuronal cell sizes. Using quantitative image and transcardially perfused with picric acid- neuronal cell sizes. Using quantitative image and transcardially perfused with picric acid- neuronal cell sizes. Using quantitative image and transcardially perfused with picric acid- analysis, we observed a statistically significant paraformaldehyde fixative. Lumbar 4 DRG’s analysis, we observed a statistically significant paraformaldehyde fixative. Lumbar 4 DRG’s analysis, we observed a statistically significant paraformaldehyde fixative. Lumbar 4 DRG’s increase in AST immunoreactivity of small were removed and processed for increase in AST immunoreactivity of small were removed and processed for increase in AST immunoreactivity of small were removed and processed for sized DRG neurons after nerve crush. We immunohistochemistry using primary sized DRG neurons after nerve crush. We immunohistochemistry using primary sized DRG neurons after nerve crush. We immunohistochemistry using primary suggest that this increase is part of the antiserum: mouse anti-VGLUT2 (1/2000, suggest that this increase is part of the antiserum: mouse anti-VGLUT2 (1/2000, suggest that this increase is part of the antiserum: mouse anti-VGLUT2 (1/2000, regenerative process of C-fiber neurons. Other NeuroMab). DRG sections were observed and regenerative process of C-fiber neurons. Other NeuroMab). DRG sections were observed and regenerative process of C-fiber neurons. Other NeuroMab). DRG sections were observed and times points are needed for evaluation to photographed using an Olympus BX5 times points are needed for evaluation to photographed using an Olympus BX5 times points are needed for evaluation to photographed using an Olympus BX5 epifluorescence microscope and SPOT camera. epifluorescence microscope and SPOT camera. epifluorescence microscope and SPOT camera.

38 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 38 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 38 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

Image J (NIH) was used to evaluate VGLUT2 study, we hypothesized that GLS expression Image J (NIH) was used to evaluate VGLUT2 study, we hypothesized that GLS expression Image J (NIH) was used to evaluate VGLUT2 study, we hypothesized that GLS expression immunoreactive intensity. VGLUT2 was found would be altered in DRG neurons after sciatic immunoreactive intensity. VGLUT2 was found would be altered in DRG neurons after sciatic immunoreactive intensity. VGLUT2 was found would be altered in DRG neurons after sciatic primarily in small to medium sized (100- nerve crush and the alteration might contribute primarily in small to medium sized (100- nerve crush and the alteration might contribute primarily in small to medium sized (100- nerve crush and the alteration might contribute 800µm2) DRG neurons, although some larger the regeneration of the nerve. Unilateral sciatic 800µm2) DRG neurons, although some larger the regeneration of the nerve. Unilateral sciatic 800µm2) DRG neurons, although some larger the regeneration of the nerve. Unilateral sciatic neurons were VGLUT2 immunoreactive. At 14 nerve crush was induced in rats at midthigh neurons were VGLUT2 immunoreactive. At 14 nerve crush was induced in rats at midthigh neurons were VGLUT2 immunoreactive. At 14 nerve crush was induced in rats at midthigh days following nerve crush, VGLUT2 level and rats with skin/muscle incision were days following nerve crush, VGLUT2 level and rats with skin/muscle incision were days following nerve crush, VGLUT2 level and rats with skin/muscle incision were immunoreactivity was elevated in small DRG used as controls. At 14 days after sciatic nerve immunoreactivity was elevated in small DRG used as controls. At 14 days after sciatic nerve immunoreactivity was elevated in small DRG used as controls. At 14 days after sciatic nerve neurons (100-400µm2) and diminished in crush, rats were transcardially perfused with neurons (100-400µm2) and diminished in crush, rats were transcardially perfused with neurons (100-400µm2) and diminished in crush, rats were transcardially perfused with 2 2 2 medium sized DRG neurons (400-800µm ). picric acid-paraformaldehyde and lumbar4-5 medium sized DRG neurons (400-800µm ). picric acid-paraformaldehyde and lumbar4-5 medium sized DRG neurons (400-800µm ). picric acid-paraformaldehyde and lumbar4-5 There was no change in large neurons DRGs were collected. GLS was localized by There was no change in large neurons DRGs were collected. GLS was localized by There was no change in large neurons DRGs were collected. GLS was localized by (>800µm2). Our data indicate that glutamate immunofluorescence and evaluated by image (>800µm2). Our data indicate that glutamate immunofluorescence and evaluated by image (>800µm2). Our data indicate that glutamate immunofluorescence and evaluated by image metabolism (VGLUT2 expression) is altered in analysis with Image J (NIH). Neurons were metabolism (VGLUT2 expression) is altered in analysis with Image J (NIH). Neurons were metabolism (VGLUT2 expression) is altered in analysis with Image J (NIH). Neurons were DRG neurons during regeneration. Since separated by cell size: small (100-400µm2), DRG neurons during regeneration. Since separated by cell size: small (100-400µm2), DRG neurons during regeneration. Since separated by cell size: small (100-400µm2), VGLUT2 is used for glutamate exocytosis, it medium (400-800µm2), large (>800µm2). VGLUT2 is used for glutamate exocytosis, it medium (400-800µm2), large (>800µm2). VGLUT2 is used for glutamate exocytosis, it medium (400-800µm2), large (>800µm2). will be important to determine the fate of These sizes often correlate with C-fiber, Aδ- will be important to determine the fate of These sizes often correlate with C-fiber, Aδ- will be important to determine the fate of These sizes often correlate with C-fiber, Aδ- VGLUT2 synaptic vesicles during the fiber, and Aβ-fiber neurons, respectively. After VGLUT2 synaptic vesicles during the fiber, and Aβ-fiber neurons, respectively. After VGLUT2 synaptic vesicles during the fiber, and Aβ-fiber neurons, respectively. After regenerative process. Funded by NIH 14 days, there was a significant decrease in GLS regenerative process. Funded by NIH 14 days, there was a significant decrease in GLS regenerative process. Funded by NIH 14 days, there was a significant decrease in GLS AR047410 (KEM). in DRG neurons. Analysis based on neuronal AR047410 (KEM). in DRG neurons. Analysis based on neuronal AR047410 (KEM). in DRG neurons. Analysis based on neuronal size showed that the major decrease in GLS size showed that the major decrease in GLS size showed that the major decrease in GLS P-9 Alteration of Glutaminase In Rat expression level occurred in small-sized P-9 Alteration of Glutaminase In Rat expression level occurred in small-sized P-9 Alteration of Glutaminase In Rat expression level occurred in small-sized Dorsal Root Ganglion Neurons During The (<400µm2) cells. These results help further Dorsal Root Ganglion Neurons During The (<400µm2) cells. These results help further Dorsal Root Ganglion Neurons During The (<400µm2) cells. These results help further Regenerative Phase Following Sciatic Nerve characterize the expression of GLS after nerve Regenerative Phase Following Sciatic Nerve characterize the expression of GLS after nerve Regenerative Phase Following Sciatic Nerve characterize the expression of GLS after nerve Crush injury. Additional information is needed to Crush injury. Additional information is needed to Crush injury. Additional information is needed to understand the temporal expression pattern of understand the temporal expression pattern of understand the temporal expression pattern of Z. Zhang, S. Alothman, B. Bolt, K.E. Miller GLS and to determine the role of GLS in the Z. Zhang, S. Alothman, B. Bolt, K.E. Miller GLS and to determine the role of GLS in the Z. Zhang, S. Alothman, B. Bolt, K.E. Miller GLS and to determine the role of GLS in the Department of Anatomy and Cell regeneration process at the periphery. Funded Department of Anatomy and Cell regeneration process at the periphery. Funded Department of Anatomy and Cell regeneration process at the periphery. Funded Biology, Oklahoma State University Center for by NIH AR047410 (KEM). Biology, Oklahoma State University Center for by NIH AR047410 (KEM). Biology, Oklahoma State University Center for by NIH AR047410 (KEM). Health Sciences, Tulsa, OK 74107 Health Sciences, Tulsa, OK 74107 Health Sciences, Tulsa, OK 74107 P-10 An Immunohistochemical Analysis of P-10 An Immunohistochemical Analysis of P-10 An Immunohistochemical Analysis of Glutamate is the major neurotransmitter Various Growth-Associated Proteins In Glutamate is the major neurotransmitter Various Growth-Associated Proteins In Glutamate is the major neurotransmitter Various Growth-Associated Proteins In in nervous system and the integrity of the Regenerating Adult Rat Retinal Ganglion in nervous system and the integrity of the Regenerating Adult Rat Retinal Ganglion in nervous system and the integrity of the Regenerating Adult Rat Retinal Ganglion glutamate-glutamine cycle is important in Cells glutamate-glutamine cycle is important in Cells glutamate-glutamine cycle is important in Cells maintaining or restoring neuronal function. maintaining or restoring neuronal function. maintaining or restoring neuronal function. After peripheral nerve insult, the glutamate- A.R. Harvey, C.E. Humphries, A.T. Julian, K.L. After peripheral nerve insult, the glutamate- A.R. Harvey, C.E. Humphries, A.T. Julian, K.L. After peripheral nerve insult, the glutamate- A.R. Harvey, C.E. Humphries, A.T. Julian, K.L. glutamine cycle is challenged or compromised. Hoath, M. Hellström, Y. Hu, M.A. Pollett glutamine cycle is challenged or compromised. Hoath, M. Hellström, Y. Hu, M.A. Pollett glutamine cycle is challenged or compromised. Hoath, M. Hellström, Y. Hu, M.A. Pollett It has been reported that there is an elevation of School of Anatomy and Human Biology, It has been reported that there is an elevation of School of Anatomy and Human Biology, It has been reported that there is an elevation of School of Anatomy and Human Biology, glutamate at the site regenerating nerve fibers, The University of Western Australia, Crawley, glutamate at the site regenerating nerve fibers, The University of Western Australia, Crawley, glutamate at the site regenerating nerve fibers, The University of Western Australia, Crawley, but the source of the elevated glutamate has not WA6009, Australia but the source of the elevated glutamate has not WA6009, Australia but the source of the elevated glutamate has not WA6009, Australia been studied. Glutaminase (GLS) is the enzyme been studied. Glutaminase (GLS) is the enzyme been studied. Glutaminase (GLS) is the enzyme responsible for the conversion of glutamine to The rat visual system is often used to responsible for the conversion of glutamine to The rat visual system is often used to responsible for the conversion of glutamine to The rat visual system is often used to glutamate. Previous studies from our laboratory study the mechanisms associated with glutamate. Previous studies from our laboratory study the mechanisms associated with glutamate. Previous studies from our laboratory study the mechanisms associated with using inflammatory models show that GLS is regenerative responses in the adult central using inflammatory models show that GLS is regenerative responses in the adult central using inflammatory models show that GLS is regenerative responses in the adult central elevated in dorsal root ganglion (DRG) neurons nervous system (CNS). We examined the elevated in dorsal root ganglion (DRG) neurons nervous system (CNS). We examined the elevated in dorsal root ganglion (DRG) neurons nervous system (CNS). We examined the in the acute phase of inflammation, followed by expression of a panel of key components of in the acute phase of inflammation, followed by expression of a panel of key components of in the acute phase of inflammation, followed by expression of a panel of key components of a decrease in soma GLS due to axonal transport various cell signalling pathways, including a decrease in soma GLS due to axonal transport various cell signalling pathways, including a decrease in soma GLS due to axonal transport various cell signalling pathways, including to the peripheral site of injury. In the current phospho-Akt, phospho-CREB, arginase-1, to the peripheral site of injury. In the current phospho-Akt, phospho-CREB, arginase-1, to the peripheral site of injury. In the current phospho-Akt, phospho-CREB, arginase-1,

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 39 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 39 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 39 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE phosphorylated ribosomal protein S6 (p-S6), the P-11 Patterns From Noise: A Data- phosphorylated ribosomal protein S6 (p-S6), the P-11 Patterns From Noise: A Data- phosphorylated ribosomal protein S6 (p-S6), the P-11 Patterns From Noise: A Data- neurotrophin receptor TrkB, growth associated Intensive Retrospective Study of Thoracic neurotrophin receptor TrkB, growth associated Intensive Retrospective Study of Thoracic neurotrophin receptor TrkB, growth associated Intensive Retrospective Study of Thoracic protein GAP-43, the immediate early gene c- SCI Laboratory Records From 1992-2003 (N protein GAP-43, the immediate early gene c- SCI Laboratory Records From 1992-2003 (N protein GAP-43, the immediate early gene c- SCI Laboratory Records From 1992-2003 (N Jun, and the anti-apoptotic protein bcl-2. We = 1400) Jun, and the anti-apoptotic protein bcl-2. We = 1400) Jun, and the anti-apoptotic protein bcl-2. We = 1400) attempted to discern differences between attempted to discern differences between attempted to discern differences between regenerating retinal ganglion cells (RGCs) and A. R. Ferguson, C. F. Guandique, A. W. Liu, J. regenerating retinal ganglion cells (RGCs) and A. R. Ferguson, C. F. Guandique, A. W. Liu, J. regenerating retinal ganglion cells (RGCs) and A. R. Ferguson, C. F. Guandique, A. W. Liu, J. viable, non-regenerating RGCs. In anesthetized L. Nielson, J. C. Bresnahan, M. S. Beattie viable, non-regenerating RGCs. In anesthetized L. Nielson, J. C. Bresnahan, M. S. Beattie viable, non-regenerating RGCs. In anesthetized L. Nielson, J. C. Bresnahan, M. S. Beattie (ketamine/xylazine) young adult rats, the left Brain and Spinal Injury Center (BASIC), (ketamine/xylazine) young adult rats, the left Brain and Spinal Injury Center (BASIC), (ketamine/xylazine) young adult rats, the left Brain and Spinal Injury Center (BASIC), optic nerve (ON) was cut and a segment of Department of Neurological Surgery, University optic nerve (ON) was cut and a segment of Department of Neurological Surgery, University optic nerve (ON) was cut and a segment of Department of Neurological Surgery, University autologous peripheral nerve (PN) grafted onto of California San Francisco, San Francisco, CA autologous peripheral nerve (PN) grafted onto of California San Francisco, San Francisco, CA autologous peripheral nerve (PN) grafted onto of California San Francisco, San Francisco, CA the cut end. Four and 11 days after surgery, the the cut end. Four and 11 days after surgery, the the cut end. Four and 11 days after surgery, the grafted eye was injected with saline (control) or Spinal cord injury (SCI) produces grafted eye was injected with saline (control) or Spinal cord injury (SCI) produces grafted eye was injected with saline (control) or Spinal cord injury (SCI) produces ciliary neurotrophic factor (CNTF) and a cell complex symptoms including disturbances in ciliary neurotrophic factor (CNTF) and a cell complex symptoms including disturbances in ciliary neurotrophic factor (CNTF) and a cell complex symptoms including disturbances in permeant cAMP analogue chlorphenylthio- mobility, sensory, and autonomic function. permeant cAMP analogue chlorphenylthio- mobility, sensory, and autonomic function. permeant cAMP analogue chlorphenylthio- mobility, sensory, and autonomic function. cAMP (CPT-cAMP) (Cui et al 2003; Park et al Despite their heterogeneity, these outcomes cAMP (CPT-cAMP) (Cui et al 2003; Park et al Despite their heterogeneity, these outcomes cAMP (CPT-cAMP) (Cui et al 2003; Park et al Despite their heterogeneity, these outcomes 2004). Surviving RGCs were visualized using often co-vary in animal models, producing a 2004). Surviving RGCs were visualized using often co-vary in animal models, producing a 2004). Surviving RGCs were visualized using often co-vary in animal models, producing a anti-βIII-tubulin antibody, and regenerating constellation of symptoms that manifest across anti-βIII-tubulin antibody, and regenerating constellation of symptoms that manifest across anti-βIII-tubulin antibody, and regenerating constellation of symptoms that manifest across RGCs identified by injecting fluorogold or fast numerous outcome measures. This suggests that RGCs identified by injecting fluorogold or fast numerous outcome measures. This suggests that RGCs identified by injecting fluorogold or fast numerous outcome measures. This suggests that blue into PN grafts 4 weeks after surgery. As SCI represents a multivariate syndrome rather blue into PN grafts 4 weeks after surgery. As SCI represents a multivariate syndrome rather blue into PN grafts 4 weeks after surgery. As SCI represents a multivariate syndrome rather expected there was increased RGC viability and than a singular deficit that can be characterized expected there was increased RGC viability and than a singular deficit that can be characterized expected there was increased RGC viability and than a singular deficit that can be characterized axonal regeneration in eyes injected with CNTF by univariate analysis (t-test; ANOVA) of a axonal regeneration in eyes injected with CNTF by univariate analysis (t-test; ANOVA) of a axonal regeneration in eyes injected with CNTF by univariate analysis (t-test; ANOVA) of a and CPT-cAMP, associated with increased single outcome. Our work uses multivariate and CPT-cAMP, associated with increased single outcome. Our work uses multivariate and CPT-cAMP, associated with increased single outcome. Our work uses multivariate expression of c-jun and GAP-43. About 90% of information-processing approaches to enable expression of c-jun and GAP-43. About 90% of information-processing approaches to enable expression of c-jun and GAP-43. About 90% of information-processing approaches to enable regenerating RGCs expressed these markers; integrative translation of stable outcome regenerating RGCs expressed these markers; integrative translation of stable outcome regenerating RGCs expressed these markers; integrative translation of stable outcome however there was variability in expression - patterns in large heterogeneous SCI datasets. however there was variability in expression - patterns in large heterogeneous SCI datasets. however there was variability in expression - patterns in large heterogeneous SCI datasets. some regenerating RGCs were not We focus on emergent patterns across many some regenerating RGCs were not We focus on emergent patterns across many some regenerating RGCs were not We focus on emergent patterns across many immunoreactive for c-jun, others negative for outcomes, rather than individual outcomes that immunoreactive for c-jun, others negative for outcomes, rather than individual outcomes that immunoreactive for c-jun, others negative for outcomes, rather than individual outcomes that GAP-43, while some surviving but not may only detect species-specific or model- GAP-43, while some surviving but not may only detect species-specific or model- GAP-43, while some surviving but not may only detect species-specific or model- regenerating RGCs could express high levels of specific changes. Our approach requires large regenerating RGCs could express high levels of specific changes. Our approach requires large regenerating RGCs could express high levels of specific changes. Our approach requires large these proteins. Similarly, there was increased datasets and sophisticated statistics that are these proteins. Similarly, there was increased datasets and sophisticated statistics that are these proteins. Similarly, there was increased datasets and sophisticated statistics that are expression of p-S6 (Park et al 2008), although uncommon in basic SCI research. We are now expression of p-S6 (Park et al 2008), although uncommon in basic SCI research. We are now expression of p-S6 (Park et al 2008), although uncommon in basic SCI research. We are now only 30-40% of regenerating RGCs were assembling a database of raw historical SCI data only 30-40% of regenerating RGCs were assembling a database of raw historical SCI data only 30-40% of regenerating RGCs were assembling a database of raw historical SCI data immunoreactive, often the larger cells. collected at multiple research centers. Our goal immunoreactive, often the larger cells. collected at multiple research centers. Our goal immunoreactive, often the larger cells. collected at multiple research centers. Our goal Expression of other growth-associated proteins is to develop a common infrastructure to enable Expression of other growth-associated proteins is to develop a common infrastructure to enable Expression of other growth-associated proteins is to develop a common infrastructure to enable was seen in both surviving and regrowing large-scale data analysis and data-sharing for the was seen in both surviving and regrowing large-scale data analysis and data-sharing for the was seen in both surviving and regrowing large-scale data analysis and data-sharing for the RGCs, more frequently in the latter, but again SCI research community. As proof-of-concept, RGCs, more frequently in the latter, but again SCI research community. As proof-of-concept, RGCs, more frequently in the latter, but again SCI research community. As proof-of-concept, expression was inconsistent. Taken together, the the present abstract reports the process required expression was inconsistent. Taken together, the the present abstract reports the process required expression was inconsistent. Taken together, the the present abstract reports the process required results suggest that individual adult RGCs can to assemble a database and perform multivariate results suggest that individual adult RGCs can to assemble a database and perform multivariate results suggest that individual adult RGCs can to assemble a database and perform multivariate harness more than one potential growth pattern-detection from raw laboratory records harness more than one potential growth pattern-detection from raw laboratory records harness more than one potential growth pattern-detection from raw laboratory records promoting signalling pathway when initiating a from one laboratory. We manually curated promoting signalling pathway when initiating a from one laboratory. We manually curated promoting signalling pathway when initiating a from one laboratory. We manually curated regenerative response. 746,164 data points encoding 66 variables and regenerative response. 746,164 data points encoding 66 variables and regenerative response. 746,164 data points encoding 66 variables and Cui Q et al (2003) Mol Cell Neurosci 22:49-61. multiple time-points, from >1400 subjects with Cui Q et al (2003) Mol Cell Neurosci 22:49-61. multiple time-points, from >1400 subjects with Cui Q et al (2003) Mol Cell Neurosci 22:49-61. multiple time-points, from >1400 subjects with Park K et al (2004) J Neurosci 24:10806-15. thoracic contusion injuries. Outcome variables Park K et al (2004) J Neurosci 24:10806-15. thoracic contusion injuries. Outcome variables Park K et al (2004) J Neurosci 24:10806-15. thoracic contusion injuries. Outcome variables Park K et al (2008) Science 322:963-6. included locomotor performance, autonomic Park K et al (2008) Science 322:963-6. included locomotor performance, autonomic Park K et al (2008) Science 322:963-6. included locomotor performance, autonomic measures (blood pressure, heart rate, bladder measures (blood pressure, heart rate, bladder measures (blood pressure, heart rate, bladder function), and spinal histology. The goal was to function), and spinal histology. The goal was to function), and spinal histology. The goal was to

40 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 40 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 40 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE build a fully annotated record for each subject to generate an average response from a number of build a fully annotated record for each subject to generate an average response from a number of build a fully annotated record for each subject to generate an average response from a number of enable multivariate syndromic knowledge- trials: what is lost is information contained enable multivariate syndromic knowledge- trials: what is lost is information contained enable multivariate syndromic knowledge- trials: what is lost is information contained discovery. We then applied non-linear principal within H-reflex variability. We have analyzed discovery. We then applied non-linear principal within H-reflex variability. We have analyzed discovery. We then applied non-linear principal within H-reflex variability. We have analyzed components analysis (CAT-PCA) using both time-independent and time-dependent components analysis (CAT-PCA) using both time-independent and time-dependent components analysis (CAT-PCA) using both time-independent and time-dependent appropriate link functions for each outcome variability to determine the effects on the H- appropriate link functions for each outcome variability to determine the effects on the H- appropriate link functions for each outcome variability to determine the effects on the H- within the multiscale dataset. Despite data reflex of complete spinal transection, as well as within the multiscale dataset. Despite data reflex of complete spinal transection, as well as within the multiscale dataset. Despite data reflex of complete spinal transection, as well as heterogeneity, we were able to identify of more selective lesions using a serotonergic heterogeneity, we were able to identify of more selective lesions using a serotonergic heterogeneity, we were able to identify of more selective lesions using a serotonergic consistent syndromic features in this diverse neurotoxin, 5,7-dihydroxytrypatime. We used consistent syndromic features in this diverse neurotoxin, 5,7-dihydroxytrypatime. We used consistent syndromic features in this diverse neurotoxin, 5,7-dihydroxytrypatime. We used archive, representing distinct therapeutic targets classic measures of time-independent variability archive, representing distinct therapeutic targets classic measures of time-independent variability archive, representing distinct therapeutic targets classic measures of time-independent variability from the intersection of histology, locomotor, (such as variance, the difference of an individual from the intersection of histology, locomotor, (such as variance, the difference of an individual from the intersection of histology, locomotor, (such as variance, the difference of an individual and autonomic outcomes. Through this data- H-reflex from the mean) and time-dependent and autonomic outcomes. Through this data- H-reflex from the mean) and time-dependent and autonomic outcomes. Through this data- H-reflex from the mean) and time-dependent intensive approach we hope to provide decision variability (using spectral analysis). If intensive approach we hope to provide decision variability (using spectral analysis). If intensive approach we hope to provide decision variability (using spectral analysis). If support for translational comparisons and variability arises due to effects of random noise support for translational comparisons and variability arises due to effects of random noise support for translational comparisons and variability arises due to effects of random noise bench-to-bedside testing of experimental on H-reflex circuitry generated by descending bench-to-bedside testing of experimental on H-reflex circuitry generated by descending bench-to-bedside testing of experimental on H-reflex circuitry generated by descending therapeutics. Support: NS067092, NS069537, and local neurons, then the variability is not therapeutics. Support: NS067092, NS069537, and local neurons, then the variability is not therapeutics. Support: NS067092, NS069537, and local neurons, then the variability is not AG032518, NS038079, NS31193 time-dependent. If the injected noise instead has AG032518, NS038079, NS31193 time-dependent. If the injected noise instead has AG032518, NS038079, NS31193 time-dependent. If the injected noise instead has some underlying trend, then the variability is some underlying trend, then the variability is some underlying trend, then the variability is P-12 Signals From Noise: Reflex Variability time-dependent or ‘fractal’. Fractal properties P-12 Signals From Noise: Reflex Variability time-dependent or ‘fractal’. Fractal properties P-12 Signals From Noise: Reflex Variability time-dependent or ‘fractal’. Fractal properties Analysis As A Diagnostic Tool In Spinal occur in several biological systems and may be Analysis As A Diagnostic Tool In Spinal occur in several biological systems and may be Analysis As A Diagnostic Tool In Spinal occur in several biological systems and may be Cord Injury functionally/prognostically relevant. H-reflex Cord Injury functionally/prognostically relevant. H-reflex Cord Injury functionally/prognostically relevant. H-reflex ‘fractalness’ is diminished in people with SCI, ‘fractalness’ is diminished in people with SCI, ‘fractalness’ is diminished in people with SCI, J.J. Cragg1, L.M. Ramer1, A.P. van Stolk1, and but has never been examined in an animal J.J. Cragg1, L.M. Ramer1, A.P. van Stolk1, and but has never been examined in an animal J.J. Cragg1, L.M. Ramer1, A.P. van Stolk1, and but has never been examined in an animal M.S. Ramer1 model, precluding eventual dissection of M.S. Ramer1 model, precluding eventual dissection of M.S. Ramer1 model, precluding eventual dissection of 1International Collaboration on Repair underlying mechanisms. These studies of H- 1International Collaboration on Repair underlying mechanisms. These studies of H- 1International Collaboration on Repair underlying mechanisms. These studies of H- Discoveries (ICORD), University of British reflex variability will set the stage for Discoveries (ICORD), University of British reflex variability will set the stage for Discoveries (ICORD), University of British reflex variability will set the stage for Columbia, Vancouver, Canada development of a novel, non-invasive tool for Columbia, Vancouver, Canada development of a novel, non-invasive tool for Columbia, Vancouver, Canada development of a novel, non-invasive tool for unraveling SCI-induced changes following SCI. unraveling SCI-induced changes following SCI. unraveling SCI-induced changes following SCI. Simple, non-invasive and quantifiable Simple, non-invasive and quantifiable Simple, non-invasive and quantifiable measures are essential to assess outcomes of P-13 Evaluation Of Conduction Through measures are essential to assess outcomes of P-13 Evaluation Of Conduction Through measures are essential to assess outcomes of P-13 Evaluation Of Conduction Through spinal cord injury (SCI) to track spontaneous Motor Pathways: Using Evoked Potentials In spinal cord injury (SCI) to track spontaneous Motor Pathways: Using Evoked Potentials In spinal cord injury (SCI) to track spontaneous Motor Pathways: Using Evoked Potentials In changes and evaluate the efficacy of treatment. Non-Human Primates changes and evaluate the efficacy of treatment. Non-Human Primates changes and evaluate the efficacy of treatment. Non-Human Primates Current clinical methods suffer from their semi- Current clinical methods suffer from their semi- Current clinical methods suffer from their semi- quantitative nature and operator inconsistencies. F. Benavides1, D. Tovar1, A. Santamaria1, L. quantitative nature and operator inconsistencies. F. Benavides1, D. Tovar1, A. Santamaria1, L. quantitative nature and operator inconsistencies. F. Benavides1, D. Tovar1, A. Santamaria1, L. The result is an inability to objectively detect Guada1, J. Guest1-2. The result is an inability to objectively detect Guada1, J. Guest1-2. The result is an inability to objectively detect Guada1, J. Guest1-2. small but potentially significant changes. Here, 1The Miami Project to Cure Paralysis, small but potentially significant changes. Here, 1The Miami Project to Cure Paralysis, small but potentially significant changes. Here, 1The Miami Project to Cure Paralysis, we have evaluated the variability in the 2Department of Neurological Surgery University we have evaluated the variability in the 2Department of Neurological Surgery University we have evaluated the variability in the 2Department of Neurological Surgery University monosynaptic H-reflex as a novel method to of Miami Miller School of Medicine. monosynaptic H-reflex as a novel method to of Miami Miller School of Medicine. monosynaptic H-reflex as a novel method to of Miami Miller School of Medicine. assess changes in spinal circuitry following SCI. assess changes in spinal circuitry following SCI. assess changes in spinal circuitry following SCI. The H-reflex is a widely-used clinical Introduction: Translation of spinal cord The H-reflex is a widely-used clinical Introduction: Translation of spinal cord The H-reflex is a widely-used clinical Introduction: Translation of spinal cord electrophysiological tool; it manifests as a repair strategies from preclinical models to electrophysiological tool; it manifests as a repair strategies from preclinical models to electrophysiological tool; it manifests as a repair strategies from preclinical models to compound muscle action potential upon humans is aided when comparable non-invasive compound muscle action potential upon humans is aided when comparable non-invasive compound muscle action potential upon humans is aided when comparable non-invasive electrical stimulation of a motor nerve. As assessment methodologies can be applied. electrical stimulation of a motor nerve. As assessment methodologies can be applied. electrical stimulation of a motor nerve. As assessment methodologies can be applied. striking as day-to-day and subject-to-subject Trans-cranial electrical stimulation (TES) and striking as day-to-day and subject-to-subject Trans-cranial electrical stimulation (TES) and striking as day-to-day and subject-to-subject Trans-cranial electrical stimulation (TES) and differences is the variability of H-reflex size trans-cranial magnetic stimulation (TMS) are differences is the variability of H-reflex size trans-cranial magnetic stimulation (TMS) are differences is the variability of H-reflex size trans-cranial magnetic stimulation (TMS) are during an individual recording session. The alternate methods to assess the integrity of during an individual recording session. The alternate methods to assess the integrity of during an individual recording session. The alternate methods to assess the integrity of usual procedure for reporting H-wave data is to motor pathways in disease states. It is usual procedure for reporting H-wave data is to motor pathways in disease states. It is usual procedure for reporting H-wave data is to motor pathways in disease states. It is

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 41 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 41 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 41 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE particularly useful to be able to stimulate the G. Stein.1, J. Ankerne2, O. Semler3, S. particularly useful to be able to stimulate the G. Stein.1, J. Ankerne2, O. Semler3, S. particularly useful to be able to stimulate the G. Stein.1, J. Ankerne2, O. Semler3, S. motor cortex of one hemisphere.Theoretically, Angelova4, M. Ashrafi2, L. Eisel2, R. Harrach2, motor cortex of one hemisphere.Theoretically, Angelova4, M. Ashrafi2, L. Eisel2, R. Harrach2, motor cortex of one hemisphere.Theoretically, Angelova4, M. Ashrafi2, L. Eisel2, R. Harrach2, axonal repair of the corticospinal tract mediated G. Schempf2, K. Wellmann2, F. Wirth2, O. axonal repair of the corticospinal tract mediated G. Schempf2, K. Wellmann2, F. Wirth2, O. axonal repair of the corticospinal tract mediated G. Schempf2, K. Wellmann2, F. Wirth2, O. via cell transplantation and subsequent Ozsoy5, U. Ozsoy6, E. Schönau3, A. Irintchev7, via cell transplantation and subsequent Ozsoy5, U. Ozsoy6, E. Schönau3, A. Irintchev7, via cell transplantation and subsequent Ozsoy5, U. Ozsoy6, E. Schönau3, A. Irintchev7, remyelination could be detected with these D. Angelov2 remyelination could be detected with these D. Angelov2 remyelination could be detected with these D. Angelov2 techniques. Our objective was to establish 1Department of Orthopedics and Trauma techniques. Our objective was to establish 1Department of Orthopedics and Trauma techniques. Our objective was to establish 1Department of Orthopedics and Trauma reproducible methodology in monkeys using Surgery, University of Cologne, Germany; reproducible methodology in monkeys using Surgery, University of Cologne, Germany; reproducible methodology in monkeys using Surgery, University of Cologne, Germany; TES and TMS and to compare the utility of the 2Department of Anatomy I, University of TES and TMS and to compare the utility of the 2Department of Anatomy I, University of TES and TMS and to compare the utility of the 2Department of Anatomy I, University of two methods in order to obtain baseline data in Cologne, Germany; 3Children University two methods in order to obtain baseline data in Cologne, Germany; 3Children University two methods in order to obtain baseline data in Cologne, Germany; 3Children University ongoing experiments in which the unilateral Hospital, University of Cologne, Germany; ongoing experiments in which the unilateral Hospital, University of Cologne, Germany; ongoing experiments in which the unilateral Hospital, University of Cologne, Germany; medullary pyramid is lesioned. Then after 4Jean-Uhrmacher Institute for ENT-Research, medullary pyramid is lesioned. Then after 4Jean-Uhrmacher Institute for ENT-Research, medullary pyramid is lesioned. Then after 4Jean-Uhrmacher Institute for ENT-Research, neurological recovery plateau, the ability of a University of Cologne, Germany; 5Department neurological recovery plateau, the ability of a University of Cologne, Germany; 5Department neurological recovery plateau, the ability of a University of Cologne, Germany; 5Department cell transplant to repair demyelinated axons is of Physiology, Faculty of Medicine, Akdeniz cell transplant to repair demyelinated axons is of Physiology, Faculty of Medicine, Akdeniz cell transplant to repair demyelinated axons is of Physiology, Faculty of Medicine, Akdeniz assessed. Lateralized cortical stimulation is University, Antalya, Turkey; 6Department of assessed. Lateralized cortical stimulation is University, Antalya, Turkey; 6Department of assessed. Lateralized cortical stimulation is University, Antalya, Turkey; 6Department of highly desirable to test collateral sprouting after Anatomy, Faculty of Medicine, Akdeniz highly desirable to test collateral sprouting after Anatomy, Faculty of Medicine, Akdeniz highly desirable to test collateral sprouting after Anatomy, Faculty of Medicine, Akdeniz cellular therapy. We hypothesized that focalized University, Antalya, Turkey; 7Department of cellular therapy. We hypothesized that focalized University, Antalya, Turkey; 7Department of cellular therapy. We hypothesized that focalized University, Antalya, Turkey; 7Department of cortical stimulation resulting in selective Oto-Rhino-Laryngology, University of Jena, cortical stimulation resulting in selective Oto-Rhino-Laryngology, University of Jena, cortical stimulation resulting in selective Oto-Rhino-Laryngology, University of Jena, activation of the contra lateral limb muscles to Germany activation of the contra lateral limb muscles to Germany activation of the contra lateral limb muscles to Germany the site of stimulation could be achieved with the site of stimulation could be achieved with the site of stimulation could be achieved with TMS rather that TES in anesthetized primates. Aims and Objectives. Knowledge on the TMS rather that TES in anesthetized primates. Aims and Objectives. Knowledge on the TMS rather that TES in anesthetized primates. Aims and Objectives. Knowledge on the Methodology: Primates were assessed under morphological grounds of motor deficits after Methodology: Primates were assessed under morphological grounds of motor deficits after Methodology: Primates were assessed under morphological grounds of motor deficits after propofol anesthesia. TES: Scalp stimulation traumatic spinal cord injury (SCI) is crucial for propofol anesthesia. TES: Scalp stimulation traumatic spinal cord injury (SCI) is crucial for propofol anesthesia. TES: Scalp stimulation traumatic spinal cord injury (SCI) is crucial for was obtained by subdermal placement of understanding the mechanisms of functional was obtained by subdermal placement of understanding the mechanisms of functional was obtained by subdermal placement of understanding the mechanisms of functional monoplolar needle electrodes, trains with recovery. In the present study we looked for monoplolar needle electrodes, trains with recovery. In the present study we looked for monoplolar needle electrodes, trains with recovery. In the present study we looked for increasing intensity values where delivered in a correlations between objective functional increasing intensity values where delivered in a correlations between objective functional increasing intensity values where delivered in a correlations between objective functional range of 150V–300V. TMS: a focal eight- (single-frame video motion analysis, range of 150V–300V. TMS: a focal eight- (single-frame video motion analysis, range of 150V–300V. TMS: a focal eight- (single-frame video motion analysis, shaped coil used, single pulse stimuli were electrophysiological measurements) and shaped coil used, single pulse stimuli were electrophysiological measurements) and shaped coil used, single pulse stimuli were electrophysiological measurements) and delivered increasing gradually the percentage of morphological (lesion scar volume) parameters delivered increasing gradually the percentage of morphological (lesion scar volume) parameters delivered increasing gradually the percentage of morphological (lesion scar volume) parameters stimulation. EMG: needle electrodes were after SCI compression injury in rats. Materials stimulation. EMG: needle electrodes were after SCI compression injury in rats. Materials stimulation. EMG: needle electrodes were after SCI compression injury in rats. Materials placed in the myotomes of fore and hind limbs and Methods. Adult female Wistar rats were placed in the myotomes of fore and hind limbs and Methods. Adult female Wistar rats were placed in the myotomes of fore and hind limbs and Methods. Adult female Wistar rats were bilaterally. Thresholds were assessed for each subjected to graded compression of the spinal bilaterally. Thresholds were assessed for each subjected to graded compression of the spinal bilaterally. Thresholds were assessed for each subjected to graded compression of the spinal muscle and 6-8 consecutive stimulation trials cord at midthoracic level (Th8). Recovery of muscle and 6-8 consecutive stimulation trials cord at midthoracic level (Th8). Recovery of muscle and 6-8 consecutive stimulation trials cord at midthoracic level (Th8). Recovery of were performed. Recordings were obtained with locomotion was analyzed using video were performed. Recordings were obtained with locomotion was analyzed using video were performed. Recordings were obtained with locomotion was analyzed using video similar filtering/amplifying parameters. recordings of beam walking and inclined ladder similar filtering/amplifying parameters. recordings of beam walking and inclined ladder similar filtering/amplifying parameters. recordings of beam walking and inclined ladder Stimulation arrays were optimized to isolate climbing. Four functional parameters were used: Stimulation arrays were optimized to isolate climbing. Four functional parameters were used: Stimulation arrays were optimized to isolate climbing. Four functional parameters were used: stimulation to the motor cortex of one the foot-stepping angle (FSA), the rump-height stimulation to the motor cortex of one the foot-stepping angle (FSA), the rump-height stimulation to the motor cortex of one the foot-stepping angle (FSA), the rump-height hemisphere. Conclusions: Reliable TES and index (RHI) estimating paw placement and body hemisphere. Conclusions: Reliable TES and index (RHI) estimating paw placement and body hemisphere. Conclusions: Reliable TES and index (RHI) estimating paw placement and body TMS methodology was established. TMS weight support, respectively, the number of TMS methodology was established. TMS weight support, respectively, the number of TMS methodology was established. TMS weight support, respectively, the number of stimulation was more effective to selectively correct ladder steps (CLS) assessing skilled stimulation was more effective to selectively correct ladder steps (CLS) assessing skilled stimulation was more effective to selectively correct ladder steps (CLS) assessing skilled stimulate unilateral motor cortex in primates hindlimb movements and the locomotor rating stimulate unilateral motor cortex in primates hindlimb movements and the locomotor rating stimulate unilateral motor cortex in primates hindlimb movements and the locomotor rating under anesthesia. score of Basso, Beattie and Bresnahan (BBB). under anesthesia. score of Basso, Beattie and Bresnahan (BBB). under anesthesia. score of Basso, Beattie and Bresnahan (BBB). Results and Discussion. Together with the Results and Discussion. Together with the Results and Discussion. Together with the P-14 Correlates of Motor Dysfunction After enhanced H-reflex responses at frequencies P-14 Correlates of Motor Dysfunction After enhanced H-reflex responses at frequencies P-14 Correlates of Motor Dysfunction After enhanced H-reflex responses at frequencies Spinal Cord Injury In Rats. between 0.1 and 5.0 Hz these parameters Spinal Cord Injury In Rats. between 0.1 and 5.0 Hz these parameters Spinal Cord Injury In Rats. between 0.1 and 5.0 Hz these parameters correlated with the scar volume (measured in correlated with the scar volume (measured in correlated with the scar volume (measured in Cresyl Violet-stained longitudinal sections Cresyl Violet-stained longitudinal sections Cresyl Violet-stained longitudinal sections

42 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 42 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 42 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE through the lesion site) showing significant Immunohistochemical techniques were through the lesion site) showing significant Immunohistochemical techniques were through the lesion site) showing significant Immunohistochemical techniques were differences between moderately and severely used to assess average forelimb muscle fiber differences between moderately and severely used to assess average forelimb muscle fiber differences between moderately and severely used to assess average forelimb muscle fiber injured rats at 1-12 weeks after SCI. cross sectional area (CSA) and the injured rats at 1-12 weeks after SCI. cross sectional area (CSA) and the injured rats at 1-12 weeks after SCI. cross sectional area (CSA) and the Conclusion. The use of these objective neuroanatomical circuitry of the forelimb was Conclusion. The use of these objective neuroanatomical circuitry of the forelimb was Conclusion. The use of these objective neuroanatomical circuitry of the forelimb was functional and morphological measures provides assessed using retrograde transneuronal tracing functional and morphological measures provides assessed using retrograde transneuronal tracing functional and morphological measures provides assessed using retrograde transneuronal tracing a time- and cost-efficient opportunity for techniques. Initial results indicate dramatic a time- and cost-efficient opportunity for techniques. Initial results indicate dramatic a time- and cost-efficient opportunity for techniques. Initial results indicate dramatic versatile and reliable functional evaluations in reductions in ipsilateral forelimb use (p<0.01) versatile and reliable functional evaluations in reductions in ipsilateral forelimb use (p<0.01) versatile and reliable functional evaluations in reductions in ipsilateral forelimb use (p<0.01) both severely and moderately impaired rats and muscle fiber CSA (p<0.05) at 1-week post- both severely and moderately impaired rats and muscle fiber CSA (p<0.05) at 1-week post- both severely and moderately impaired rats and muscle fiber CSA (p<0.05) at 1-week post- combining clinical assessment with precise C2Hx. By 8-weeks post-injury, improvements combining clinical assessment with precise C2Hx. By 8-weeks post-injury, improvements combining clinical assessment with precise C2Hx. By 8-weeks post-injury, improvements numerical measures. in ipsilateral forelimb use (p<0.01) and numerical measures. in ipsilateral forelimb use (p<0.01) and numerical measures. in ipsilateral forelimb use (p<0.01) and increased muscle fiber CSA (p<0.05) were increased muscle fiber CSA (p<0.05) were increased muscle fiber CSA (p<0.05) were P-15 Neuromuscular Plasticity In The Rat observed. Preliminary results from tracing P-15 Neuromuscular Plasticity In The Rat observed. Preliminary results from tracing P-15 Neuromuscular Plasticity In The Rat observed. Preliminary results from tracing Forelimb After High Cervical Spinal Cord studies in uninjured animals revealed first-order Forelimb After High Cervical Spinal Cord studies in uninjured animals revealed first-order Forelimb After High Cervical Spinal Cord studies in uninjured animals revealed first-order Injury labeling of forelimb motoneurons in the lateral Injury labeling of forelimb motoneurons in the lateral Injury labeling of forelimb motoneurons in the lateral ventral horn of the cervical spinal cord as well ventral horn of the cervical spinal cord as well ventral horn of the cervical spinal cord as well E.J. Gonzalez-Rothi1, 2, R.A Federico2, A. Daly3, as labeling of second-order interneurons. These E.J. Gonzalez-Rothi1, 2, R.A Federico2, A. Daly3, as labeling of second-order interneurons. These E.J. Gonzalez-Rothi1, 2, R.A Federico2, A. Daly3, as labeling of second-order interneurons. These A. Rombola3, B.E. O’Steen, initial results indicate substantial muscular A. Rombola3, B.E. O’Steen, initial results indicate substantial muscular A. Rombola3, B.E. O’Steen, initial results indicate substantial muscular K.V. Vandenborne2, P.J. Reier3, D.D. Fuller2, phenotypic remodeling and modest recovery in K.V. Vandenborne2, P.J. Reier3, D.D. Fuller2, phenotypic remodeling and modest recovery in K.V. Vandenborne2, P.J. Reier3, D.D. Fuller2, phenotypic remodeling and modest recovery in M.A. Lane3 forelimb function following cSCI, and ongoing M.A. Lane3 forelimb function following cSCI, and ongoing M.A. Lane3 forelimb function following cSCI, and ongoing 1College of Public Health and Health studies are exploring the neuroanatomical 1College of Public Health and Health studies are exploring the neuroanatomical 1College of Public Health and Health studies are exploring the neuroanatomical Professions Graduate Program in circuitry associated with forelimb dysfunction Professions Graduate Program in circuitry associated with forelimb dysfunction Professions Graduate Program in circuitry associated with forelimb dysfunction Rehabilitation Science; 2Department of Physical and recovery after injury. The pattern of Rehabilitation Science; 2Department of Physical and recovery after injury. The pattern of Rehabilitation Science; 2Department of Physical and recovery after injury. The pattern of Therapy; 3Department of Neuroscience, forelimb recovery appears to parallel the Therapy; 3Department of Neuroscience, forelimb recovery appears to parallel the Therapy; 3Department of Neuroscience, forelimb recovery appears to parallel the McKnight Brain Institute, University of Florida, previously documented recovery of ipsilateral McKnight Brain Institute, University of Florida, previously documented recovery of ipsilateral McKnight Brain Institute, University of Florida, previously documented recovery of ipsilateral Gainesville, FL phrenic motor output following C2Hx. These Gainesville, FL phrenic motor output following C2Hx. These Gainesville, FL phrenic motor output following C2Hx. These experiments are the first to examine the experiments are the first to examine the experiments are the first to examine the Injury to the cervical spinal cord (cSCI) combined muscular and neuroanatomical Injury to the cervical spinal cord (cSCI) combined muscular and neuroanatomical Injury to the cervical spinal cord (cSCI) combined muscular and neuroanatomical can lead to devastating consequences, including mechanisms underlying neuroplasticity and can lead to devastating consequences, including mechanisms underlying neuroplasticity and can lead to devastating consequences, including mechanisms underlying neuroplasticity and impaired upper extremity (UE) function. recovery of function following cSCI and may impaired upper extremity (UE) function. recovery of function following cSCI and may impaired upper extremity (UE) function. recovery of function following cSCI and may Although some capacity for functional aid in identifying potential therapeutic targets Although some capacity for functional aid in identifying potential therapeutic targets Although some capacity for functional aid in identifying potential therapeutic targets improvement has been demonstrated, the extent for rehabilitation interventions. improvement has been demonstrated, the extent for rehabilitation interventions. improvement has been demonstrated, the extent for rehabilitation interventions. of recovery is limited and the underlying Funding: Paralyzed Veterans of America of recovery is limited and the underlying Funding: Paralyzed Veterans of America of recovery is limited and the underlying Funding: Paralyzed Veterans of America mechanisms are ill defined. In contrast, Research Foundation (ML), NIH 1R21 mechanisms are ill defined. In contrast, Research Foundation (ML), NIH 1R21 mechanisms are ill defined. In contrast, Research Foundation (ML), NIH 1R21 functional recovery within the phrenic HL104294-01 (DDF) NIH RO1 NS054025 functional recovery within the phrenic HL104294-01 (DDF) NIH RO1 NS054025 functional recovery within the phrenic HL104294-01 (DDF) NIH RO1 NS054025 (respiratory) motor system is well characterized (PJR), NIH T32HD04730 (KV), Foundation for (respiratory) motor system is well characterized (PJR), NIH T32HD04730 (KV), Foundation for (respiratory) motor system is well characterized (PJR), NIH T32HD04730 (KV), Foundation for and the neural substrates associated with this Physical Therapy PODS II grant (EGR), a grant and the neural substrates associated with this Physical Therapy PODS II grant (EGR), a grant and the neural substrates associated with this Physical Therapy PODS II grant (EGR), a grant plasticity have been studied in great detail using from the Bryan Robinson Neuroscience plasticity have been studied in great detail using from the Bryan Robinson Neuroscience plasticity have been studied in great detail using from the Bryan Robinson Neuroscience a well-established rodent model of cSCI, the Endowment Fund (EGR), and a grant from the a well-established rodent model of cSCI, the Endowment Fund (EGR), and a grant from the a well-established rodent model of cSCI, the Endowment Fund (EGR), and a grant from the lateral C2 spinal cord hemisection (C2Hx). The College of Public Health and Health and Health lateral C2 spinal cord hemisection (C2Hx). The College of Public Health and Health and Health lateral C2 spinal cord hemisection (C2Hx). The College of Public Health and Health and Health present works exmines the muscular and Professions-University of Florida (EGR) present works exmines the muscular and Professions-University of Florida (EGR) present works exmines the muscular and Professions-University of Florida (EGR) neuroanatomical substrates underlying upper neuroanatomical substrates underlying upper neuroanatomical substrates underlying upper extremity dysfunction and recovery after C2Hx P-16 In Vivo Testing Of Candidate Genes extremity dysfunction and recovery after C2Hx P-16 In Vivo Testing Of Candidate Genes extremity dysfunction and recovery after C2Hx P-16 In Vivo Testing Of Candidate Genes in adult Sprague-Dawley rats. Gross forelimb To Promote Neuron-Intrinsic Growth Ability in adult Sprague-Dawley rats. Gross forelimb To Promote Neuron-Intrinsic Growth Ability in adult Sprague-Dawley rats. Gross forelimb To Promote Neuron-Intrinsic Growth Ability motor function was assessed prior to, and at 1- And Axon Regeneration In The Injured motor function was assessed prior to, and at 1- And Axon Regeneration In The Injured motor function was assessed prior to, and at 1- And Axon Regeneration In The Injured and 8-weeks post-injury using the limb-use Spinal Cord and 8-weeks post-injury using the limb-use Spinal Cord and 8-weeks post-injury using the limb-use Spinal Cord asymmetry (cylinder) test. asymmetry (cylinder) test. asymmetry (cylinder) test.

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 43 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 43 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 43 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

M.G. Blackmore1, Z. Wang3, P. Zheng2, C. in vivo model of spinal cord injury, both singly M.G. Blackmore1, Z. Wang3, P. Zheng2, C. in vivo model of spinal cord injury, both singly M.G. Blackmore1, Z. Wang3, P. Zheng2, C. in vivo model of spinal cord injury, both singly Shields2, V.P. Lemmon3, J.L. Bixby3 and in combination, these experiments will help Shields2, V.P. Lemmon3, J.L. Bixby3 and in combination, these experiments will help Shields2, V.P. Lemmon3, J.L. Bixby3 and in combination, these experiments will help 1Department of Biomedical Sciences, clarify the neuron-intrinsic control of axon 1Department of Biomedical Sciences, clarify the neuron-intrinsic control of axon 1Department of Biomedical Sciences, clarify the neuron-intrinsic control of axon Marquette University, Milwaukee, WI; 2Norton regeneration and identify new therapeutic Marquette University, Milwaukee, WI; 2Norton regeneration and identify new therapeutic Marquette University, Milwaukee, WI; 2Norton regeneration and identify new therapeutic Neurological Institute, Louisville, KY; 3The avenues to promote axon regeneration in the Neurological Institute, Louisville, KY; 3The avenues to promote axon regeneration in the Neurological Institute, Louisville, KY; 3The avenues to promote axon regeneration in the Miami Project to Cure Paralysis, University of injured CNS. Miami Project to Cure Paralysis, University of injured CNS. Miami Project to Cure Paralysis, University of injured CNS. Miami Miller School of Medicine, Miami, FL Miami Miller School of Medicine, Miami, FL Miami Miller School of Medicine, Miami, FL P-17 Allogeneic And Autologous Schwann P-17 Allogeneic And Autologous Schwann P-17 Allogeneic And Autologous Schwann Axon regeneration in the adult central Cell Grafts In A Porcine SCI Contusion Axon regeneration in the adult central Cell Grafts In A Porcine SCI Contusion Axon regeneration in the adult central Cell Grafts In A Porcine SCI Contusion nervous system (CNS) fails in part because Model: Immune Response And CNS nervous system (CNS) fails in part because Model: Immune Response And CNS nervous system (CNS) fails in part because Model: Immune Response And CNS many CNS neurons possess an intrinsically low Integration many CNS neurons possess an intrinsically low Integration many CNS neurons possess an intrinsically low Integration capacity for rapid axon growth. Identifying and capacity for rapid axon growth. Identifying and capacity for rapid axon growth. Identifying and reversing neuron-intrinsic constraints on axon A. Santamaria1, F. Benavides1, L. Guada1, G. reversing neuron-intrinsic constraints on axon A. Santamaria1, F. Benavides1, L. Guada1, G. reversing neuron-intrinsic constraints on axon A. Santamaria1, F. Benavides1, L. Guada1, G. growth is critical to restore CNS function after Athauda1, H. Levene1, J. Solano2, J. Guest1 growth is critical to restore CNS function after Athauda1, H. Levene1, J. Solano2, J. Guest1 growth is critical to restore CNS function after Athauda1, H. Levene1, J. Solano2, J. Guest1 axon tracts are disrupted by injury or disease. 1Neurological Surgery and The Miami axon tracts are disrupted by injury or disease. 1Neurological Surgery and The Miami axon tracts are disrupted by injury or disease. 1Neurological Surgery and The Miami Axon growth ability declines dramatically as Project to Cure Paralysis, 2Pediatric Critical Axon growth ability declines dramatically as Project to Cure Paralysis, 2Pediatric Critical Axon growth ability declines dramatically as Project to Cure Paralysis, 2Pediatric Critical neurons age postnatally, likely due to the both Care, University of Miami, Miller School of neurons age postnatally, likely due to the both Care, University of Miami, Miller School of neurons age postnatally, likely due to the both Care, University of Miami, Miller School of downregulation of growth-promoting genes and Medicine. downregulation of growth-promoting genes and Medicine. downregulation of growth-promoting genes and Medicine. upregulation of growth-suppressive genes upregulation of growth-suppressive genes upregulation of growth-suppressive genes within CNS neurons. Using a screening Introduction: Transplanted Schwann within CNS neurons. Using a screening Introduction: Transplanted Schwann within CNS neurons. Using a screening Introduction: Transplanted Schwann approach, we previously identified a number of cells (SC) have reparative effects after SCI. An approach, we previously identified a number of cells (SC) have reparative effects after SCI. An approach, we previously identified a number of cells (SC) have reparative effects after SCI. An developmentally regulated genes that either autologous approach to human application in developmentally regulated genes that either autologous approach to human application in developmentally regulated genes that either autologous approach to human application in enhance or suppress neurite outgrowth when SCI is limited by the time required to culture enhance or suppress neurite outgrowth when SCI is limited by the time required to culture enhance or suppress neurite outgrowth when SCI is limited by the time required to culture overexpressed in primary neurons in culture. To sufficient cells from donor nerve. We assessed overexpressed in primary neurons in culture. To sufficient cells from donor nerve. We assessed overexpressed in primary neurons in culture. To sufficient cells from donor nerve. We assessed test gene function in vivo we are now using whether allogeneic SC promote similar test gene function in vivo we are now using whether allogeneic SC promote similar test gene function in vivo we are now using whether allogeneic SC promote similar adeno-associated viral particles (AAV) to reparative effects to autologous SC with cell adeno-associated viral particles (AAV) to reparative effects to autologous SC with cell adeno-associated viral particles (AAV) to reparative effects to autologous SC with cell overexpress or knock down candidate genes in survival, axonal sprouting, myelination and overexpress or knock down candidate genes in survival, axonal sprouting, myelination and overexpress or knock down candidate genes in survival, axonal sprouting, myelination and corticospinal tract (CST) neurons in adult mice, inflammation as endpoints. Methods: Twenty corticospinal tract (CST) neurons in adult mice, inflammation as endpoints. Methods: Twenty corticospinal tract (CST) neurons in adult mice, inflammation as endpoints. Methods: Twenty followed by transection of CST axons in the Yucatan minipigs underwent T8 laminectomy followed by transection of CST axons in the Yucatan minipigs underwent T8 laminectomy followed by transection of CST axons in the Yucatan minipigs underwent T8 laminectomy cervical spinal cord. Using virally-produced and contusion. Autografts were produced from a cervical spinal cord. Using virally-produced and contusion. Autografts were produced from a cervical spinal cord. Using virally-produced and contusion. Autografts were produced from a EGFP as a tracer, we quantify axonal dieback superficial femoral nerve, SC were purified and EGFP as a tracer, we quantify axonal dieback superficial femoral nerve, SC were purified and EGFP as a tracer, we quantify axonal dieback superficial femoral nerve, SC were purified and and regeneration by transduced CST axons. We labeled with GFP lentivirus at P1. Three and regeneration by transduced CST axons. We labeled with GFP lentivirus at P1. Three and regeneration by transduced CST axons. We labeled with GFP lentivirus at P1. Three have tested a number of candidate genes, volumes 50, 100 or 150 µl of 200,000 SC/µl have tested a number of candidate genes, volumes 50, 100 or 150 µl of 200,000 SC/µl have tested a number of candidate genes, volumes 50, 100 or 150 µl of 200,000 SC/µl including cytoskeletal interacting proteins (P2) were injected at 21d to mimic preparation including cytoskeletal interacting proteins (P2) were injected at 21d to mimic preparation including cytoskeletal interacting proteins (P2) were injected at 21d to mimic preparation (doublecortin / DCX), regulators of small time in a human trial. Pigs survived 3d to six (doublecortin / DCX), regulators of small time in a human trial. Pigs survived 3d to six (doublecortin / DCX), regulators of small time in a human trial. Pigs survived 3d to six GTPases (NGEF / Ephexin), transcription weeks. Tissue sections were stained with LFB- GTPases (NGEF / Ephexin), transcription weeks. Tissue sections were stained with LFB- GTPases (NGEF / Ephexin), transcription weeks. Tissue sections were stained with LFB- factors (multiple members of the Kruppel-like H/E and immunostained for several relevant factors (multiple members of the Kruppel-like H/E and immunostained for several relevant factors (multiple members of the Kruppel-like H/E and immunostained for several relevant family / KLFs), as well as previously identified markers. Results: In allogeneic and family / KLFs), as well as previously identified markers. Results: In allogeneic and family / KLFs), as well as previously identified markers. Results: In allogeneic and regulators of axon growth (PTEN and SOCS3). autologously transplanted pigs the lesion cavity regulators of axon growth (PTEN and SOCS3). autologously transplanted pigs the lesion cavity regulators of axon growth (PTEN and SOCS3). autologously transplanted pigs the lesion cavity We demonstrate effective gene overexpression, showed extensive macrophage activity, We demonstrate effective gene overexpression, showed extensive macrophage activity, We demonstrate effective gene overexpression, showed extensive macrophage activity, and, importantly, highly effective knockdown of astrocytes enclose cavities and extend processes and, importantly, highly effective knockdown of astrocytes enclose cavities and extend processes and, importantly, highly effective knockdown of astrocytes enclose cavities and extend processes candidate genes in CST neurons in vivo. into the epicenter. The largest injections caused candidate genes in CST neurons in vivo. into the epicenter. The largest injections caused candidate genes in CST neurons in vivo. into the epicenter. The largest injections caused Furthermore, we have identified a KLF-based secondary cavities and pressure extrusion along Furthermore, we have identified a KLF-based secondary cavities and pressure extrusion along Furthermore, we have identified a KLF-based secondary cavities and pressure extrusion along gene manipulation that promotes CST grey-white matter boundaries rostral and caudal gene manipulation that promotes CST grey-white matter boundaries rostral and caudal gene manipulation that promotes CST grey-white matter boundaries rostral and caudal regeneration in the injured spinal cord. By to the injury epicenter. Abundant peripheral regeneration in the injured spinal cord. By to the injury epicenter. Abundant peripheral regeneration in the injured spinal cord. By to the injury epicenter. Abundant peripheral testing large numbers of candidate genes in an nerve fascicles entered the injured cord testing large numbers of candidate genes in an nerve fascicles entered the injured cord testing large numbers of candidate genes in an nerve fascicles entered the injured cord

44 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 44 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 44 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE especially in grafted animals. Marked Wistar rats (300g) received a complete especially in grafted animals. Marked Wistar rats (300g) received a complete especially in grafted animals. Marked Wistar rats (300g) received a complete lymphocytic and polymorphonuclear transection of the spinal cord at the third (T3) or lymphocytic and polymorphonuclear transection of the spinal cord at the third (T3) or lymphocytic and polymorphonuclear transection of the spinal cord at the third (T3) or perivascular infiltration was present in allografts tenth (T10) thoracic segment or sham injury perivascular infiltration was present in allografts tenth (T10) thoracic segment or sham injury perivascular infiltration was present in allografts tenth (T10) thoracic segment or sham injury but also detected in some autografts, one animal (durotomy without SCI). After 1-12 weeks, but also detected in some autografts, one animal (durotomy without SCI). After 1-12 weeks, but also detected in some autografts, one animal (durotomy without SCI). After 1-12 weeks, showed large lymphocytic nodules related to the dorsal root ganglia (DRGs) and spinal cord were showed large lymphocytic nodules related to the dorsal root ganglia (DRGs) and spinal cord were showed large lymphocytic nodules related to the dorsal root ganglia (DRGs) and spinal cord were implant. Close apposition of astrocytes and harvested and analyzed immunohistochemically implant. Close apposition of astrocytes and harvested and analyzed immunohistochemically implant. Close apposition of astrocytes and harvested and analyzed immunohistochemically grafted SC was present in all transplants. to examine soma size of TRPV1-positive grafted SC was present in all transplants. to examine soma size of TRPV1-positive grafted SC was present in all transplants. to examine soma size of TRPV1-positive Demyelinated axons and autologous SC were afferents and density of their central projections. Demyelinated axons and autologous SC were afferents and density of their central projections. Demyelinated axons and autologous SC were afferents and density of their central projections. aligned even at early post transplant times, and TRPV-1-positive nociceptors exhibited aligned even at early post transplant times, and TRPV-1-positive nociceptors exhibited aligned even at early post transplant times, and TRPV-1-positive nociceptors exhibited the number of ensheathed axons and axonal hypertrophy after T3 SCI. Nociceptor the number of ensheathed axons and axonal hypertrophy after T3 SCI. Nociceptor the number of ensheathed axons and axonal hypertrophy after T3 SCI. Nociceptor sprouts was greater in longer survivals. hypertrophy only occurred in DRGs below the sprouts was greater in longer survivals. hypertrophy only occurred in DRGs below the sprouts was greater in longer survivals. hypertrophy only occurred in DRGs below the Conclusions: Survival of autologous level of SCI, and was more pronounced after Conclusions: Survival of autologous level of SCI, and was more pronounced after Conclusions: Survival of autologous level of SCI, and was more pronounced after transplanted SC was superior to allogeneic SC. high thoracic (T3) SCI. Hypertrophy was transplanted SC was superior to allogeneic SC. high thoracic (T3) SCI. Hypertrophy was transplanted SC was superior to allogeneic SC. high thoracic (T3) SCI. Hypertrophy was Host SC response from nerve roots into the pronounced in DRGs far distal to SCI, and Host SC response from nerve roots into the pronounced in DRGs far distal to SCI, and Host SC response from nerve roots into the pronounced in DRGs far distal to SCI, and lesion was extensive. SC promoted restructuring occurred in DRGs comprised of predominately lesion was extensive. SC promoted restructuring occurred in DRGs comprised of predominately lesion was extensive. SC promoted restructuring occurred in DRGs comprised of predominately of injury cavities via axonal sprouting and somatic (L4,L5) and visceral (L6,S1) afferents. of injury cavities via axonal sprouting and somatic (L4,L5) and visceral (L6,S1) afferents. of injury cavities via axonal sprouting and somatic (L4,L5) and visceral (L6,S1) afferents. myelination. The unexpected finding of TRPV-1-expressing nociceptors also appeared myelination. The unexpected finding of TRPV-1-expressing nociceptors also appeared myelination. The unexpected finding of TRPV-1-expressing nociceptors also appeared substantial lymphocytic activity including to sprout within the lumbar dorsal horn: the area substantial lymphocytic activity including to sprout within the lumbar dorsal horn: the area substantial lymphocytic activity including to sprout within the lumbar dorsal horn: the area nodules in both allo and autografts is under occupied by TRPV-1-positive axons was nodules in both allo and autografts is under occupied by TRPV-1-positive axons was nodules in both allo and autografts is under occupied by TRPV-1-positive axons was further study. increased one month after SCI. further study. increased one month after SCI. further study. increased one month after SCI. TRPV-1-expressing nociceptors respond TRPV-1-expressing nociceptors respond TRPV-1-expressing nociceptors respond P-18 Hot ‘n‘ bothered: the role of TRPV1- to SCI by undergoing somal hypertrophy and P-18 Hot ‘n‘ bothered: the role of TRPV1- to SCI by undergoing somal hypertrophy and P-18 Hot ‘n‘ bothered: the role of TRPV1- to SCI by undergoing somal hypertrophy and positive sensory neurons in autonomic expanding their central terminals in the lumbar positive sensory neurons in autonomic expanding their central terminals in the lumbar positive sensory neurons in autonomic expanding their central terminals in the lumbar dysreflexia dorsal horn. Recent data from another dysreflexia dorsal horn. Recent data from another dysreflexia dorsal horn. Recent data from another laboratory demonstrates that this anatomical laboratory demonstrates that this anatomical laboratory demonstrates that this anatomical L. M. Ramer,1,2; A. P. van Stolk1, J. A. Inskip, plasticity is accompanied by spontaneous L. M. Ramer,1,2; A. P. van Stolk1, J. A. Inskip, plasticity is accompanied by spontaneous L. M. Ramer,1,2; A. P. van Stolk1, J. A. Inskip, plasticity is accompanied by spontaneous 1,2; M. S. Ramer1,2; J. D. Steeves1; A. V. activity in TRPV-1-positive afferents caudal to 1,2; M. S. Ramer1,2; J. D. Steeves1; A. V. activity in TRPV-1-positive afferents caudal to 1,2; M. S. Ramer1,2; J. D. Steeves1; A. V. activity in TRPV-1-positive afferents caudal to Krassioukov1,3,4 SCI. We are currently using capsaicin to Krassioukov1,3,4 SCI. We are currently using capsaicin to Krassioukov1,3,4 SCI. We are currently using capsaicin to 1ICORD (International Collaboration on determine the contribution of TRPV-1-positive 1ICORD (International Collaboration on determine the contribution of TRPV-1-positive 1ICORD (International Collaboration on determine the contribution of TRPV-1-positive Repair Discoveries), University of British afferents to the development of AD following Repair Discoveries), University of British afferents to the development of AD following Repair Discoveries), University of British afferents to the development of AD following Columbia (UBC),Vancouver, BC, Canada; high-thoracic SCI. Columbia (UBC),Vancouver, BC, Canada; high-thoracic SCI. Columbia (UBC),Vancouver, BC, Canada; high-thoracic SCI. 2Department of Zoology, UBC ; 3GF Strong 2Department of Zoology, UBC ; 3GF Strong 2Department of Zoology, UBC ; 3GF Strong Rehabilitation Centre, Vancouver; 4Department P-19 Myelin Gene Regulatory Factor Rehabilitation Centre, Vancouver; 4Department P-19 Myelin Gene Regulatory Factor Rehabilitation Centre, Vancouver; 4Department P-19 Myelin Gene Regulatory Factor of Medicine, UBC Knockout Delays Functional Recovery From of Medicine, UBC Knockout Delays Functional Recovery From of Medicine, UBC Knockout Delays Functional Recovery From Spinal Cord Injury Spinal Cord Injury Spinal Cord Injury TRPV1 is expressed by a subpopulation TRPV1 is expressed by a subpopulation TRPV1 is expressed by a subpopulation of sensory neurons. It is activated by heat G. J. Duncan1, J. R. Plemel1, B. J. Hilton1, J. of sensory neurons. It is activated by heat G. J. Duncan1, J. R. Plemel1, B. J. Hilton1, J. of sensory neurons. It is activated by heat G. J. Duncan1, J. R. Plemel1, B. J. Hilton1, J. (>43ºC), low pH, and capsaicin (the pungent Liu1, J. K. Kramer1, J. Kim1, S. Mao1, and W. (>43ºC), low pH, and capsaicin (the pungent Liu1, J. K. Kramer1, J. Kim1, S. Mao1, and W. (>43ºC), low pH, and capsaicin (the pungent Liu1, J. K. Kramer1, J. Kim1, S. Mao1, and W. ingredient in hot chili peppers), and has Tetzlaff1,2. ingredient in hot chili peppers), and has Tetzlaff1,2. ingredient in hot chili peppers), and has Tetzlaff1,2. emerged as a promising target for the treatment 1ICORD (International Collaboration on emerged as a promising target for the treatment 1ICORD (International Collaboration on emerged as a promising target for the treatment 1ICORD (International Collaboration on of pain. Both pain and autonomic dysreflexia Repair Discoveries), 2Department of Zoology of pain. Both pain and autonomic dysreflexia Repair Discoveries), 2Department of Zoology of pain. Both pain and autonomic dysreflexia Repair Discoveries), 2Department of Zoology that develop in the wake of SCI have been University of British Columbia (UBC), that develop in the wake of SCI have been University of British Columbia (UBC), that develop in the wake of SCI have been University of British Columbia (UBC), attributed to maladaptive sensory plasticity. We Vancouver, BC, Canada attributed to maladaptive sensory plasticity. We Vancouver, BC, Canada attributed to maladaptive sensory plasticity. We Vancouver, BC, Canada hypothesize that TRPV-1-positive afferents hypothesize that TRPV-1-positive afferents hypothesize that TRPV-1-positive afferents contribute to the development of autonomic Spinal cord injury causes death of contribute to the development of autonomic Spinal cord injury causes death of contribute to the development of autonomic Spinal cord injury causes death of dysreflexia (AD). oligodendrocytes and subsequent demyelination dysreflexia (AD). oligodendrocytes and subsequent demyelination dysreflexia (AD). oligodendrocytes and subsequent demyelination

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 45 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 45 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 45 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE of axons. Myelin replacement occurs by the 3Department of Pediatrics Case Western of axons. Myelin replacement occurs by the 3Department of Pediatrics Case Western of axons. Myelin replacement occurs by the 3Department of Pediatrics Case Western recruitment of oligodendrocyte precursors Reserve University, Cleveland, OH recruitment of oligodendrocyte precursors Reserve University, Cleveland, OH recruitment of oligodendrocyte precursors Reserve University, Cleveland, OH (OPCs) followed by their maturation into (OPCs) followed by their maturation into (OPCs) followed by their maturation into remyelinating oligodendrocytes. The role of this The in vivo character of immune remyelinating oligodendrocytes. The role of this The in vivo character of immune remyelinating oligodendrocytes. The role of this The in vivo character of immune regenerative process and its contribution to mediated secondary axonal dieback after regenerative process and its contribution to mediated secondary axonal dieback after regenerative process and its contribution to mediated secondary axonal dieback after functional motor recovery following spinal cord traumatic spinal cord injury in is not known. functional motor recovery following spinal cord traumatic spinal cord injury in is not known. functional motor recovery following spinal cord traumatic spinal cord injury in is not known. injury (SCI) has never been tested directly. To Studies of interactions between DRG neurons injury (SCI) has never been tested directly. To Studies of interactions between DRG neurons injury (SCI) has never been tested directly. To Studies of interactions between DRG neurons test the role of remyelination in the spontaneous and macrophages in culture show a cell-cell test the role of remyelination in the spontaneous and macrophages in culture show a cell-cell test the role of remyelination in the spontaneous and macrophages in culture show a cell-cell recovery following SCI, we removed a contact mediated interaction that causes a recovery following SCI, we removed a contact mediated interaction that causes a recovery following SCI, we removed a contact mediated interaction that causes a transcriptional regulator, known as myelin gene dramatic retracting response by the neuron transcriptional regulator, known as myelin gene dramatic retracting response by the neuron transcriptional regulator, known as myelin gene dramatic retracting response by the neuron regulatory factor (MRF) that is necessary for the (Horn and Busch et al. 2008). Although these regulatory factor (MRF) that is necessary for the (Horn and Busch et al. 2008). Although these regulatory factor (MRF) that is necessary for the (Horn and Busch et al. 2008). Although these maturation of OPCs into myelinating cell types are in contact in tissue, this type of maturation of OPCs into myelinating cell types are in contact in tissue, this type of maturation of OPCs into myelinating cell types are in contact in tissue, this type of oligodendrocytes. To remove MRF we injected dramatic retraction does not occur. Time lapse oligodendrocytes. To remove MRF we injected dramatic retraction does not occur. Time lapse oligodendrocytes. To remove MRF we injected dramatic retraction does not occur. Time lapse a cre-expressing adeno-associated virus 5 multi-photon imaging methods provide a a cre-expressing adeno-associated virus 5 multi-photon imaging methods provide a a cre-expressing adeno-associated virus 5 multi-photon imaging methods provide a (AAV5) into the spinal cord of mice that were powerful tool for observing these cellular (AAV5) into the spinal cord of mice that were powerful tool for observing these cellular (AAV5) into the spinal cord of mice that were powerful tool for observing these cellular either heterozygous or homozygous for floxed interactions in real time in intact tissue with either heterozygous or homozygous for floxed interactions in real time in intact tissue with either heterozygous or homozygous for floxed interactions in real time in intact tissue with MRF two weeks prior to a thoracic crush injury. minimal disruption and high resolution. MRF two weeks prior to a thoracic crush injury. minimal disruption and high resolution. MRF two weeks prior to a thoracic crush injury. minimal disruption and high resolution. AAV5 was capable of infecting OPCs, as Animals with genetically expressed fluorescent AAV5 was capable of infecting OPCs, as Animals with genetically expressed fluorescent AAV5 was capable of infecting OPCs, as Animals with genetically expressed fluorescent indicated by co-labelling of virally expressed proteins allow us to observe cellular structures. indicated by co-labelling of virally expressed proteins allow us to observe cellular structures. indicated by co-labelling of virally expressed proteins allow us to observe cellular structures. GFP with OPC markers PDGFαR and Olig2 at Yellow fluorescent protein expressed in a GFP with OPC markers PDGFαR and Olig2 at Yellow fluorescent protein expressed in a GFP with OPC markers PDGFαR and Olig2 at Yellow fluorescent protein expressed in a the time of injury. This suggests that MRF was neuronally restricted manner under the Thy-1 the time of injury. This suggests that MRF was neuronally restricted manner under the Thy-1 the time of injury. This suggests that MRF was neuronally restricted manner under the Thy-1 removed in a subset of OPCs prior to SCI. promoter (Feng et al. 2000) labels single axons removed in a subset of OPCs prior to SCI. promoter (Feng et al. 2000) labels single axons removed in a subset of OPCs prior to SCI. promoter (Feng et al. 2000) labels single axons After injury, floxed MRF infected with Cre- in the living animal. Green fluorescent protein After injury, floxed MRF infected with Cre- in the living animal. Green fluorescent protein After injury, floxed MRF infected with Cre- in the living animal. Green fluorescent protein expressing AAV5had a delayed behavioural expressed in place of the fractalkine receptor expressing AAV5had a delayed behavioural expressed in place of the fractalkine receptor expressing AAV5had a delayed behavioural expressed in place of the fractalkine receptor recovery on the Basso Mouse Scale. Co- CX3CR1 (Jung et al. 2000) allows for the recovery on the Basso Mouse Scale. Co- CX3CR1 (Jung et al. 2000) allows for the recovery on the Basso Mouse Scale. Co- CX3CR1 (Jung et al. 2000) allows for the labelling of the mature oligodendrocyte marker observation of monocytic cells and microglia. labelling of the mature oligodendrocyte marker observation of monocytic cells and microglia. labelling of the mature oligodendrocyte marker observation of monocytic cells and microglia. CC1 and viral eGFP was assessed to determine Multi-photon in vivo imaging has been used to CC1 and viral eGFP was assessed to determine Multi-photon in vivo imaging has been used to CC1 and viral eGFP was assessed to determine Multi-photon in vivo imaging has been used to if OPC maturation was impaired in adult mice characterize axonal dieback from a dorsal if OPC maturation was impaired in adult mice characterize axonal dieback from a dorsal if OPC maturation was impaired in adult mice characterize axonal dieback from a dorsal by MRF knockout. The delayed behavioural column crush injury in these transgenic mice by MRF knockout. The delayed behavioural column crush injury in these transgenic mice by MRF knockout. The delayed behavioural column crush injury in these transgenic mice recovery suggests an important role for MRF in over a period of several days. We have recovery suggests an important role for MRF in over a period of several days. We have recovery suggests an important role for MRF in over a period of several days. We have the spontaneous motor recovery following observed infiltration and movement of CX3CR1 the spontaneous motor recovery following observed infiltration and movement of CX3CR1 the spontaneous motor recovery following observed infiltration and movement of CX3CR1 spinal cord injury. It is also the first GFP positive cells in the parenchyma of the spinal cord injury. It is also the first GFP positive cells in the parenchyma of the spinal cord injury. It is also the first GFP positive cells in the parenchyma of the demonstration that MRF has a role in the CNS lesion and in the subarachnoid space. Axons demonstration that MRF has a role in the CNS lesion and in the subarachnoid space. Axons demonstration that MRF has a role in the CNS lesion and in the subarachnoid space. Axons beyond regulating strictly developmental with retraction bulbs die back from the lesion by beyond regulating strictly developmental with retraction bulbs die back from the lesion by beyond regulating strictly developmental with retraction bulbs die back from the lesion by myelination. a membrane blebbing mechanism, also seen in myelination. a membrane blebbing mechanism, also seen in myelination. a membrane blebbing mechanism, also seen in This research is supported by the Multiple response to physical contact by a CX3CR1 This research is supported by the Multiple response to physical contact by a CX3CR1 This research is supported by the Multiple response to physical contact by a CX3CR1 Sclerosis Society of Canada. positive cell. Undisturbed axonal retraction Sclerosis Society of Canada. positive cell. Undisturbed axonal retraction Sclerosis Society of Canada. positive cell. Undisturbed axonal retraction balls are static after lesion formation for long balls are static after lesion formation for long balls are static after lesion formation for long P-20 In Vivo Real Time Observations of periods of time. Large, phagocytic, strongly P-20 In Vivo Real Time Observations of periods of time. Large, phagocytic, strongly P-20 In Vivo Real Time Observations of periods of time. Large, phagocytic, strongly Immune Cells And Neurons In Traumatic CX3CR1 positive cells are also static after Immune Cells And Neurons In Traumatic CX3CR1 positive cells are also static after Immune Cells And Neurons In Traumatic CX3CR1 positive cells are also static after Spinal Cord Injury In The Mouse injury. Understanding the in vivo cellular Spinal Cord Injury In The Mouse injury. Understanding the in vivo cellular Spinal Cord Injury In The Mouse injury. Understanding the in vivo cellular interactions involved in this secondary axonal interactions involved in this secondary axonal interactions involved in this secondary axonal T. A. Evans1, D. S. Barkauskas2, A. Y. Huang3, injury may lead to candidates for clinical T. A. Evans1, D. S. Barkauskas2, A. Y. Huang3, injury may lead to candidates for clinical T. A. Evans1, D. S. Barkauskas2, A. Y. Huang3, injury may lead to candidates for clinical J. Silver1 treatment. J. Silver1 treatment. J. Silver1 treatment. 1 Department of Neuroscience, Busch SA and Horn KP et al. J 1 Department of Neuroscience, Busch SA and Horn KP et al. J 1 Department of Neuroscience, Busch SA and Horn KP et al. J 2Department of Biomedical Engineering, Neurosci 29:9967–9976. 2Department of Biomedical Engineering, Neurosci 29:9967–9976. 2Department of Biomedical Engineering, Neurosci 29:9967–9976.

46 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 46 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 46 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

Feng G et al. 2000. Neuron 28(1):41-51. towards a Th2 phenotype when the CST was Feng G et al. 2000. Neuron 28(1):41-51. towards a Th2 phenotype when the CST was Feng G et al. 2000. Neuron 28(1):41-51. towards a Th2 phenotype when the CST was Jung S et al. 2000. Mol Cell Biol 20(11):4106- lesioned. These findings suggest that CD4+ T Jung S et al. 2000. Mol Cell Biol 20(11):4106- lesioned. These findings suggest that CD4+ T Jung S et al. 2000. Mol Cell Biol 20(11):4106- lesioned. These findings suggest that CD4+ T 14. cells activated by trauma-associated antigens 14. cells activated by trauma-associated antigens 14. cells activated by trauma-associated antigens Funding NINDS NS35713 to JS. mediate NT-3-induced axonal sprouting. Funding NINDS NS35713 to JS. mediate NT-3-induced axonal sprouting. Funding NINDS NS35713 to JS. mediate NT-3-induced axonal sprouting. Dana Foundation Brain and Immuno-Imaging Supported by the Christopher and Dana Reeve Dana Foundation Brain and Immuno-Imaging Supported by the Christopher and Dana Reeve Dana Foundation Brain and Immuno-Imaging Supported by the Christopher and Dana Reeve Award to AYH. Foundation, the Craig H. Neilsen Foundation, Award to AYH. Foundation, the Craig H. Neilsen Foundation, Award to AYH. Foundation, the Craig H. Neilsen Foundation, Mission Connect, and the Department of Mission Connect, and the Department of Mission Connect, and the Department of P-21 The Presence of Cd4+ T Cells Is Veterans Affairs. P-21 The Presence of Cd4+ T Cells Is Veterans Affairs. P-21 The Presence of Cd4+ T Cells Is Veterans Affairs. Required For Nt-3-Induced Axonal Required For Nt-3-Induced Axonal Required For Nt-3-Induced Axonal Sprouting In The Injured Spinal Cord P-22 Characterizing The Effect Of Sprouting In The Injured Spinal Cord P-22 Characterizing The Effect Of Sprouting In The Injured Spinal Cord P-22 Characterizing The Effect Of Neurotrauma On Spinal Cord And Dorsal Neurotrauma On Spinal Cord And Dorsal Neurotrauma On Spinal Cord And Dorsal C.Qin1,2 and H.D. Shine1-4 Root Ganglion Vasculature C.Qin1,2 and H.D. Shine1-4 Root Ganglion Vasculature C.Qin1,2 and H.D. Shine1-4 Root Ganglion Vasculature 1Cell and Gene Therapy, 2Neuroscience, 1Cell and Gene Therapy, 2Neuroscience, 1Cell and Gene Therapy, 2Neuroscience, and 3Molecular and Cellular Biology, Baylor M.A. Crawford1,2 and M.S. Ramer1,3 and 3Molecular and Cellular Biology, Baylor M.A. Crawford1,2 and M.S. Ramer1,3 and 3Molecular and Cellular Biology, Baylor M.A. Crawford1,2 and M.S. Ramer1,3 College of Medicine, and the 4Michael E. 1International Collaboration on Repair College of Medicine, and the 4Michael E. 1International Collaboration on Repair College of Medicine, and the 4Michael E. 1International Collaboration on Repair DeBakey VA Medical Center, Houston, Texas Discoveries (ICORD), 2Graduate Program in DeBakey VA Medical Center, Houston, Texas Discoveries (ICORD), 2Graduate Program in DeBakey VA Medical Center, Houston, Texas Discoveries (ICORD), 2Graduate Program in Neuroscience, 3Department of Zoology, the Neuroscience, 3Department of Zoology, the Neuroscience, 3Department of Zoology, the Previously, we reported that over- University of British Columbia, Vancouver, Previously, we reported that over- University of British Columbia, Vancouver, Previously, we reported that over- University of British Columbia, Vancouver, expression of Neurotrophin-3 (NT-3) promoted Canada. expression of Neurotrophin-3 (NT-3) promoted Canada. expression of Neurotrophin-3 (NT-3) promoted Canada. axonal sprouting in the injured rat spinal cord axonal sprouting in the injured rat spinal cord axonal sprouting in the injured rat spinal cord but only when acute inflammatory responses Along with other groups, we have shown but only when acute inflammatory responses Along with other groups, we have shown but only when acute inflammatory responses Along with other groups, we have shown were present. Axonal sprouting was not that macrophages invade dorsal root ganglia and were present. Axonal sprouting was not that macrophages invade dorsal root ganglia and were present. Axonal sprouting was not that macrophages invade dorsal root ganglia and observed when NT-3 over-expression was the spinal cord after spinal cord and peripheral observed when NT-3 over-expression was the spinal cord after spinal cord and peripheral observed when NT-3 over-expression was the spinal cord after spinal cord and peripheral delayed 4 months after injury when the nerve injury. Additionally, recent findings show delayed 4 months after injury when the nerve injury. Additionally, recent findings show delayed 4 months after injury when the nerve injury. Additionally, recent findings show inflammation had subsided. We observed that that macrophages guide endothelial tip cells in inflammation had subsided. We observed that that macrophages guide endothelial tip cells in inflammation had subsided. We observed that that macrophages guide endothelial tip cells in activation of CD4+ T cells in the spinal cord angiogenesis. We hypothesize, therefore, that activation of CD4+ T cells in the spinal cord angiogenesis. We hypothesize, therefore, that activation of CD4+ T cells in the spinal cord angiogenesis. We hypothesize, therefore, that coincided with axonal sprouting suggesting that areas of the nervous system subject to an influx coincided with axonal sprouting suggesting that areas of the nervous system subject to an influx coincided with axonal sprouting suggesting that areas of the nervous system subject to an influx they might participate in the NT-3-induced of macrophages after injury will also display they might participate in the NT-3-induced of macrophages after injury will also display they might participate in the NT-3-induced of macrophages after injury will also display neuroplasticity. To test this, we compared NT-3- injury-induced angiogenesis. In a rat model of neuroplasticity. To test this, we compared NT-3- injury-induced angiogenesis. In a rat model of neuroplasticity. To test this, we compared NT-3- injury-induced angiogenesis. In a rat model of induced neuroplasticity in nude rats lacking T3 complete transection spinal cord injury and induced neuroplasticity in nude rats lacking T3 complete transection spinal cord injury and induced neuroplasticity in nude rats lacking T3 complete transection spinal cord injury and functional T cells, rats heterozygous for the using immunohistochemistry, we have found an functional T cells, rats heterozygous for the using immunohistochemistry, we have found an functional T cells, rats heterozygous for the using immunohistochemistry, we have found an mutation that had functional T cells, nude rats increased capillary network density in L4 and mutation that had functional T cells, nude rats increased capillary network density in L4 and mutation that had functional T cells, nude rats increased capillary network density in L4 and grafted with CD4+ T cells, and nude rats grafted L5 dorsal root ganglia 35 days after injury. We grafted with CD4+ T cells, and nude rats grafted L5 dorsal root ganglia 35 days after injury. We grafted with CD4+ T cells, and nude rats grafted L5 dorsal root ganglia 35 days after injury. We with CD8+ T cells. After a unilateral lesion of are also interested in describing the three- with CD8+ T cells. After a unilateral lesion of are also interested in describing the three- with CD8+ T cells. After a unilateral lesion of are also interested in describing the three- the corticospinal tract (CST) NT-3 was over- dimensional morphology of vascular networks the corticospinal tract (CST) NT-3 was over- dimensional morphology of vascular networks the corticospinal tract (CST) NT-3 was over- dimensional morphology of vascular networks expressed in lesioned side of the lumbar spinal in the nervous system before and after expressed in lesioned side of the lumbar spinal in the nervous system before and after expressed in lesioned side of the lumbar spinal in the nervous system before and after cord by transducing motoneurons with an neurotrauma. To accomplish this, we are using cord by transducing motoneurons with an neurotrauma. To accomplish this, we are using cord by transducing motoneurons with an neurotrauma. To accomplish this, we are using adenoviral vector carrying the NT-3 gene. Three the vascular casting technique. This method adenoviral vector carrying the NT-3 gene. Three the vascular casting technique. This method adenoviral vector carrying the NT-3 gene. Three the vascular casting technique. This method weeks later we measured the number of axons involves perfusing the animal with a fluorescent weeks later we measured the number of axons involves perfusing the animal with a fluorescent weeks later we measured the number of axons involves perfusing the animal with a fluorescent that sprouted from the unlesioned CST into the resin that hardens to form a cast after injection. that sprouted from the unlesioned CST into the resin that hardens to form a cast after injection. that sprouted from the unlesioned CST into the resin that hardens to form a cast after injection. denervated side toward the source of NT-3. The The resulting casts are dissected out, imaged denervated side toward the source of NT-3. The The resulting casts are dissected out, imaged denervated side toward the source of NT-3. The The resulting casts are dissected out, imaged degree of sprouting was significantly greater in with confocal microscopy and analyzed with 3D degree of sprouting was significantly greater in with confocal microscopy and analyzed with 3D degree of sprouting was significantly greater in with confocal microscopy and analyzed with 3D rats with functional T cells and in nude rats that software. We seek to describe these vascular rats with functional T cells and in nude rats that software. We seek to describe these vascular rats with functional T cells and in nude rats that software. We seek to describe these vascular were grafted with CD4+ T cells compared to changes to further understand spinal cord injury were grafted with CD4+ T cells compared to changes to further understand spinal cord injury were grafted with CD4+ T cells compared to changes to further understand spinal cord injury nude rats or nude rats grafted with CD8+ T cells. pathology and to uncover potential therapeutic nude rats or nude rats grafted with CD8+ T cells. pathology and to uncover potential therapeutic nude rats or nude rats grafted with CD8+ T cells. pathology and to uncover potential therapeutic Additionally, CD4+ T cells were polarized Additionally, CD4+ T cells were polarized Additionally, CD4+ T cells were polarized

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 47 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 47 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 47 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE targets related to the angiogenic response after (±0.14) in controls. Moreover, forelimb motor targets related to the angiogenic response after (±0.14) in controls. Moreover, forelimb motor targets related to the angiogenic response after (±0.14) in controls. Moreover, forelimb motor neurotrauma. performance, measured weekly, was also neurotrauma. performance, measured weekly, was also neurotrauma. performance, measured weekly, was also significantly improved. Motor test scores, significantly improved. Motor test scores, significantly improved. Motor test scores, P-23 Autonomic And Sensorimotor averaged over the last 4 weeks for stimulated P-23 Autonomic And Sensorimotor averaged over the last 4 weeks for stimulated P-23 Autonomic And Sensorimotor averaged over the last 4 weeks for stimulated Recovery From Cervical Contusion Injury Is versus control rats, were, respectively: forelimb Recovery From Cervical Contusion Injury Is versus control rats, were, respectively: forelimb Recovery From Cervical Contusion Injury Is versus control rats, were, respectively: forelimb Boosted By Midbrain Periaqueductal Gray hang-time 8.0 s (±2.0) versus 3.3 (±1.1); grip Boosted By Midbrain Periaqueductal Gray hang-time 8.0 s (±2.0) versus 3.3 (±1.1); grip Boosted By Midbrain Periaqueductal Gray hang-time 8.0 s (±2.0) versus 3.3 (±1.1); grip Stimulation. strength 440 g (±6.7) versus 110 (±2.0); Stimulation. strength 440 g (±6.7) versus 110 (±2.0); Stimulation. strength 440 g (±6.7) versus 110 (±2.0); inclined-plane stability 43.0° (±1.88) versus inclined-plane stability 43.0° (±1.88) versus inclined-plane stability 43.0° (±1.88) versus I.D. Hentall, A. Vitores, M.M. Carballosa- 40.0 (±0.93). In sum, PAG stimulation reversed I.D. Hentall, A. Vitores, M.M. Carballosa- 40.0 (±0.93). In sum, PAG stimulation reversed I.D. Hentall, A. Vitores, M.M. Carballosa- 40.0 (±0.93). In sum, PAG stimulation reversed Gonzalez both autonomic dysreflexia and forelimb motor Gonzalez both autonomic dysreflexia and forelimb motor Gonzalez both autonomic dysreflexia and forelimb motor The Miami Project to Cure Paralysis, deficits (P<0.05, all tests). Already proven safe The Miami Project to Cure Paralysis, deficits (P<0.05, all tests). Already proven safe The Miami Project to Cure Paralysis, deficits (P<0.05, all tests). Already proven safe University of Miami Miller School of Medicine, as a neurosurgical procedure in humans (for University of Miami Miller School of Medicine, as a neurosurgical procedure in humans (for University of Miami Miller School of Medicine, as a neurosurgical procedure in humans (for Miami, FL 33136. drug-refractory pain), it represents a readily Miami, FL 33136. drug-refractory pain), it represents a readily Miami, FL 33136. drug-refractory pain), it represents a readily translatable potential treatment for acute spinal translatable potential treatment for acute spinal translatable potential treatment for acute spinal Previously we found that a few days of cord injury. Previously we found that a few days of cord injury. Previously we found that a few days of cord injury. intermittent electrical stimulation in the intermittent electrical stimulation in the intermittent electrical stimulation in the hindbrain’s nucleus raphe magnus (NRM) P-24 Skin-Derived Precursors hindbrain’s nucleus raphe magnus (NRM) P-24 Skin-Derived Precursors hindbrain’s nucleus raphe magnus (NRM) P-24 Skin-Derived Precursors improves sensorimotor and anatomical recovery Differentiated Into Schwann Cells (Skp-Scs) improves sensorimotor and anatomical recovery Differentiated Into Schwann Cells (Skp-Scs) improves sensorimotor and anatomical recovery Differentiated Into Schwann Cells (Skp-Scs) in rats with thoracic contusion injuries, and that And Transplanted Eight Weeks Post Spinal in rats with thoracic contusion injuries, and that And Transplanted Eight Weeks Post Spinal in rats with thoracic contusion injuries, and that And Transplanted Eight Weeks Post Spinal the midbrain’s periaqueductal gray (PAG), a Cord Contusion Improve Recovery Of Motor the midbrain’s periaqueductal gray (PAG), a Cord Contusion Improve Recovery Of Motor the midbrain’s periaqueductal gray (PAG), a Cord Contusion Improve Recovery Of Motor major NRM input, gives similar outcomes. Function And Bladder Pathology major NRM input, gives similar outcomes. Function And Bladder Pathology major NRM input, gives similar outcomes. Function And Bladder Pathology NRM neurons are known to respond to sensory NRM neurons are known to respond to sensory NRM neurons are known to respond to sensory and chemical correlates of body trauma (e.g., P. Assinck1, S. Dworski2, J.S. Sparling3, G.J. and chemical correlates of body trauma (e.g., P. Assinck1, S. Dworski2, J.S. Sparling3, G.J. and chemical correlates of body trauma (e.g., P. Assinck1, S. Dworski2, J.S. Sparling3, G.J. pain, circulating cytokines) and to release Duncan3, D.L. Wu3, Y. Jiang3, J. Liu3, C.K. pain, circulating cytokines) and to release Duncan3, D.L. Wu3, Y. Jiang3, J. Liu3, C.K. pain, circulating cytokines) and to release Duncan3, D.L. Wu3, Y. Jiang3, J. Liu3, C.K. growth-promoting substances (e.g., serotonin, Lam3, B.K. Kwon1, F. D. Miller2, W. Tetzlaff3 growth-promoting substances (e.g., serotonin, Lam3, B.K. Kwon1, F. D. Miller2, W. Tetzlaff3 growth-promoting substances (e.g., serotonin, Lam3, B.K. Kwon1, F. D. Miller2, W. Tetzlaff3 TRH) essentially everywhere in spinal gray 1ICORD, UBC, Vancouver, BC, Canada, TRH) essentially everywhere in spinal gray 1ICORD, UBC, Vancouver, BC, Canada, TRH) essentially everywhere in spinal gray 1ICORD, UBC, Vancouver, BC, Canada, matter. We therefore suggest that the NRM is 2Hospital for Sick Children/University of matter. We therefore suggest that the NRM is 2Hospital for Sick Children/University of matter. We therefore suggest that the NRM is 2Hospital for Sick Children/University of ipso facto a generalized repair center, with Toronto, Toronto, ON, Canada, 3ICORD, ipso facto a generalized repair center, with Toronto, Toronto, ON, Canada, 3ICORD, ipso facto a generalized repair center, with Toronto, Toronto, ON, Canada, 3ICORD, actions extending beyond sensorimotor systems UBC/ICORD, Vancouver BC, BC, Canada actions extending beyond sensorimotor systems UBC/ICORD, Vancouver BC, BC, Canada actions extending beyond sensorimotor systems UBC/ICORD, Vancouver BC, BC, Canada or particular spinal segments. To support this or particular spinal segments. To support this or particular spinal segments. To support this idea, we expanded our studies to cervical Cell transplantation has emerged as a idea, we expanded our studies to cervical Cell transplantation has emerged as a idea, we expanded our studies to cervical Cell transplantation has emerged as a injuries and autonomic outcomes. The rat’s promising candidate therapy for spinal cord injuries and autonomic outcomes. The rat’s promising candidate therapy for spinal cord injuries and autonomic outcomes. The rat’s promising candidate therapy for spinal cord ventrolateral PAG received one week of injury. Our laboratories have previously shown ventrolateral PAG received one week of injury. Our laboratories have previously shown ventrolateral PAG received one week of injury. Our laboratories have previously shown stimulation (-30 µA, 1 ms, 8 Hz, alternating that Schwann cells differentiated from skin- stimulation (-30 µA, 1 ms, 8 Hz, alternating that Schwann cells differentiated from skin- stimulation (-30 µA, 1 ms, 8 Hz, alternating that Schwann cells differentiated from skin- stimulation and rest in 5-minute periods) for 12 derived precursors (SKP-SCs), when stimulation and rest in 5-minute periods) for 12 derived precursors (SKP-SCs), when stimulation and rest in 5-minute periods) for 12 derived precursors (SKP-SCs), when hours daily, starting 1-2 hours after cervical transplanted 7 days after contusion injury, hours daily, starting 1-2 hours after cervical transplanted 7 days after contusion injury, hours daily, starting 1-2 hours after cervical transplanted 7 days after contusion injury, (C5) weight-drop contusion. Five weeks post- promote histological repair and functional (C5) weight-drop contusion. Five weeks post- promote histological repair and functional (C5) weight-drop contusion. Five weeks post- promote histological repair and functional injury, colon distension by balloon catheter (4 recovery in rats (Biernaskie et al. 2007). Here, injury, colon distension by balloon catheter (4 recovery in rats (Biernaskie et al. 2007). Here, injury, colon distension by balloon catheter (4 recovery in rats (Biernaskie et al. 2007). Here, cc) under ketamine/xylazine anesthesia caused we transplanted one million SKP-SCs at 8 cc) under ketamine/xylazine anesthesia caused we transplanted one million SKP-SCs at 8 cc) under ketamine/xylazine anesthesia caused we transplanted one million SKP-SCs at 8 significantly less autonomic dysreflexia (rise in weeks post T9/T10 contusion injury and significantly less autonomic dysreflexia (rise in weeks post T9/T10 contusion injury and significantly less autonomic dysreflexia (rise in weeks post T9/T10 contusion injury and intracarotid blood pressure) in stimulated rats allowed survival until week 29. Behavioral intracarotid blood pressure) in stimulated rats allowed survival until week 29. Behavioral intracarotid blood pressure) in stimulated rats allowed survival until week 29. Behavioral (n=11) than in controls with inactive stimulators analysis shows that SKP-SC transplanted rats (n=11) than in controls with inactive stimulators analysis shows that SKP-SC transplanted rats (n=11) than in controls with inactive stimulators analysis shows that SKP-SC transplanted rats (n=8): 7.6 mm Hg (±1.4 s.e.m) versus 24.8 elicited higher BBB scores, which reached (n=8): 7.6 mm Hg (±1.4 s.e.m) versus 24.8 elicited higher BBB scores, which reached (n=8): 7.6 mm Hg (±1.4 s.e.m) versus 24.8 elicited higher BBB scores, which reached (±0.9). Noxious pressure applied to forepaws significance at week 19-21 post injury. By (±0.9). Noxious pressure applied to forepaws significance at week 19-21 post injury. By (±0.9). Noxious pressure applied to forepaws significance at week 19-21 post injury. By also gave significantly lower pressor responses histology, we found surviving SKP-SC in all also gave significantly lower pressor responses histology, we found surviving SKP-SC in all also gave significantly lower pressor responses histology, we found surviving SKP-SC in all in stimulated rats: 3.3 mm (±1.0), versus 6.4 transplanted rats at 21 weeks post in stimulated rats: 3.3 mm (±1.0), versus 6.4 transplanted rats at 21 weeks post in stimulated rats: 3.3 mm (±1.0), versus 6.4 transplanted rats at 21 weeks post

48 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 48 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 48 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE transplantation. Ki67 immunoreactivity Foundation. 4Department of Neuroscience, Case transplantation. Ki67 immunoreactivity Foundation. 4Department of Neuroscience, Case transplantation. Ki67 immunoreactivity Foundation. 4Department of Neuroscience, Case indicated very little (<0.03-0.05%) proliferative Western Reserve University, Cleveland, OH. indicated very little (<0.03-0.05%) proliferative Western Reserve University, Cleveland, OH. indicated very little (<0.03-0.05%) proliferative Western Reserve University, Cleveland, OH. activity in this chronic stage. Cellular bands of activity in this chronic stage. Cellular bands of activity in this chronic stage. Cellular bands of SKP-SCs bridged the lesion sites in Relatively few studies have focused on SKP-SCs bridged the lesion sites in Relatively few studies have focused on SKP-SCs bridged the lesion sites in Relatively few studies have focused on predominantly rostro-caudal orientation and central neuronal regeneration with the goal of predominantly rostro-caudal orientation and central neuronal regeneration with the goal of predominantly rostro-caudal orientation and central neuronal regeneration with the goal of showed good integration into the host spinal fostering recovery of efficient micturition. The showed good integration into the host spinal fostering recovery of efficient micturition. The showed good integration into the host spinal fostering recovery of efficient micturition. The cord. SKP-SC and astrocyte processes effects of peripheral nerve grafts (PNG) and cord. SKP-SC and astrocyte processes effects of peripheral nerve grafts (PNG) and cord. SKP-SC and astrocyte processes effects of peripheral nerve grafts (PNG) and interdigitated extensively at this host transplant acidic fibroblast growth factor (aFGF) interdigitated extensively at this host transplant acidic fibroblast growth factor (aFGF) interdigitated extensively at this host transplant acidic fibroblast growth factor (aFGF) interface which was crossed by numerous combined with Chondroitinase ABC (ChABC) interface which was crossed by numerous combined with Chondroitinase ABC (ChABC) interface which was crossed by numerous combined with Chondroitinase ABC (ChABC) axons; and these SKP-SC bridges were filled on bladder reflexes after complete spinal cord axons; and these SKP-SC bridges were filled on bladder reflexes after complete spinal cord axons; and these SKP-SC bridges were filled on bladder reflexes after complete spinal cord with neurofilament positive axons running transection (ST) at T8 in adult rats were studied. with neurofilament positive axons running transection (ST) at T8 in adult rats were studied. with neurofilament positive axons running transection (ST) at T8 in adult rats were studied. predominantly in rostro-caudal orientation. Rats were divided randomly into six groups: (1) predominantly in rostro-caudal orientation. Rats were divided randomly into six groups: (1) predominantly in rostro-caudal orientation. Rats were divided randomly into six groups: (1) Immunoreactivity for serotonin transporter Sham control (laminectomy only), (2) ST only, Immunoreactivity for serotonin transporter Sham control (laminectomy only), (2) ST only, Immunoreactivity for serotonin transporter Sham control (laminectomy only), (2) ST only, (SERT) or tyrosine hydroxylase revealed many (3) ST+PNG, (4) ST+aFGF+ChABC, (5) (SERT) or tyrosine hydroxylase revealed many (3) ST+PNG, (4) ST+aFGF+ChABC, (5) (SERT) or tyrosine hydroxylase revealed many (3) ST+PNG, (4) ST+aFGF+ChABC, (5) axons growing into and through these SKP-SC ST+PNG+aFGF, (6) ST+PNG+aFGF+ChABC. axons growing into and through these SKP-SC ST+PNG+aFGF, (6) ST+PNG+aFGF+ChABC. axons growing into and through these SKP-SC ST+PNG+aFGF, (6) ST+PNG+aFGF+ChABC. bridges with some crossing the distal interface. Two injections of ChABC were made near the bridges with some crossing the distal interface. Two injections of ChABC were made near the bridges with some crossing the distal interface. Two injections of ChABC were made near the Fewer axons were positive for CGRP or SP, rostral and caudal stumps of the spinal cord. Fewer axons were positive for CGRP or SP, rostral and caudal stumps of the spinal cord. Fewer axons were positive for CGRP or SP, rostral and caudal stumps of the spinal cord. markers of sensory fibers from the periphery. Urodynamics and external urethral sphincter markers of sensory fibers from the periphery. Urodynamics and external urethral sphincter markers of sensory fibers from the periphery. Urodynamics and external urethral sphincter The numbers of P0-positive fibers were electromyogram (EMG) activity were recorded The numbers of P0-positive fibers were electromyogram (EMG) activity were recorded The numbers of P0-positive fibers were electromyogram (EMG) activity were recorded significantly higher in SKP-SC transplanted six months after injury. Anterograde tracing was significantly higher in SKP-SC transplanted six months after injury. Anterograde tracing was significantly higher in SKP-SC transplanted six months after injury. Anterograde tracing was rats, indicating a stimulation of an endogenous used to evaluate axonal regeneration. rats, indicating a stimulation of an endogenous used to evaluate axonal regeneration. rats, indicating a stimulation of an endogenous used to evaluate axonal regeneration. Schwann cell repair response by SKP-SC Urodynamic data in the Schwann cell repair response by SKP-SC Urodynamic data in the Schwann cell repair response by SKP-SC Urodynamic data in the transplantation. Interestingly, in a post hoc ST+PNG+aFGF+ChABC animals was transplantation. Interestingly, in a post hoc ST+PNG+aFGF+ChABC animals was transplantation. Interestingly, in a post hoc ST+PNG+aFGF+ChABC animals was analysis, the media control treated animals show markedly improved beyond that in the other analysis, the media control treated animals show markedly improved beyond that in the other analysis, the media control treated animals show markedly improved beyond that in the other a significant increase in bladder wall thickness four injury groups. The a significant increase in bladder wall thickness four injury groups. The a significant increase in bladder wall thickness four injury groups. The as compared to the SKP-SC treated animals, ST+PNG+aFGF+ChABC group also showed as compared to the SKP-SC treated animals, ST+PNG+aFGF+ChABC group also showed as compared to the SKP-SC treated animals, ST+PNG+aFGF+ChABC group also showed suggesting improved bladder function in the significant shorter time to void and significantly suggesting improved bladder function in the significant shorter time to void and significantly suggesting improved bladder function in the significant shorter time to void and significantly transplanted group. In summary, our results improved patterns of high frequency oscillations transplanted group. In summary, our results improved patterns of high frequency oscillations transplanted group. In summary, our results improved patterns of high frequency oscillations highlight the potential of SKP-SCs as a possible of detrusor contractions (bladder pressure highlight the potential of SKP-SCs as a possible of detrusor contractions (bladder pressure highlight the potential of SKP-SCs as a possible of detrusor contractions (bladder pressure cell for autologous transplantation in the sub- tracings) during voiding than the other four cell for autologous transplantation in the sub- tracings) during voiding than the other four cell for autologous transplantation in the sub- tracings) during voiding than the other four chronic state of spinal cord injury. injury groups. This indicates that the chronic state of spinal cord injury. injury groups. This indicates that the chronic state of spinal cord injury. injury groups. This indicates that the Supported by CIHR, Canadian Stem Cell PNG+aFGF+ChABC group did not need to Supported by CIHR, Canadian Stem Cell PNG+aFGF+ChABC group did not need to Supported by CIHR, Canadian Stem Cell PNG+aFGF+ChABC group did not need to Network, and Rick Hansen Foundation. store large volumes of urine (less bladder Network, and Rick Hansen Foundation. store large volumes of urine (less bladder Network, and Rick Hansen Foundation. store large volumes of urine (less bladder incontinence and distention) to void and incontinence and distention) to void and incontinence and distention) to void and P-25 Nerve Regeneration And developed better coordination between detrusor P-25 Nerve Regeneration And developed better coordination between detrusor P-25 Nerve Regeneration And developed better coordination between detrusor Improvement In Urodynamics And External and sphincter activity, which is closer to a Improvement In Urodynamics And External and sphincter activity, which is closer to a Improvement In Urodynamics And External and sphincter activity, which is closer to a Urethral Sphincter Activity In Complete normal pattern. The ST+PNG+aFGF+ChABC Urethral Sphincter Activity In Complete normal pattern. The ST+PNG+aFGF+ChABC Urethral Sphincter Activity In Complete normal pattern. The ST+PNG+aFGF+ChABC Spinal Cord Transected Rats Treated With A group also displayed higher amplitudes and Spinal Cord Transected Rats Treated With A group also displayed higher amplitudes and Spinal Cord Transected Rats Treated With A group also displayed higher amplitudes and Peripheral Nerve Graft, Acidic Fibroblast bursting rates of sphincter EMG activity than Peripheral Nerve Graft, Acidic Fibroblast bursting rates of sphincter EMG activity than Peripheral Nerve Graft, Acidic Fibroblast bursting rates of sphincter EMG activity than Growth Factor, And Chondroitinase ABC the other injured animals. The improvement in Growth Factor, And Chondroitinase ABC the other injured animals. The improvement in Growth Factor, And Chondroitinase ABC the other injured animals. The improvement in urodynamics and EMG disappeared after spinal urodynamics and EMG disappeared after spinal urodynamics and EMG disappeared after spinal Y.-S. Lee1,2, H-H. Jiang3, M. DePaul4, C.-Y. cord re-transection in the Y.-S. Lee1,2, H-H. Jiang3, M. DePaul4, C.-Y. cord re-transection in the Y.-S. Lee1,2, H-H. Jiang3, M. DePaul4, C.-Y. cord re-transection in the Lin1,2, M. S. Damaser3, V. W. Lin2, and J. Silver4 ST+PNG+aFGF+ChABC group, suggesting that Lin1,2, M. S. Damaser3, V. W. Lin2, and J. Silver4 ST+PNG+aFGF+ChABC group, suggesting that Lin1,2, M. S. Damaser3, V. W. Lin2, and J. Silver4 ST+PNG+aFGF+ChABC group, suggesting that Departments of 1Neurosciences and supraspinal regeneration is critical for recovery. Departments of 1Neurosciences and supraspinal regeneration is critical for recovery. Departments of 1Neurosciences and supraspinal regeneration is critical for recovery. 2Physical Med & Rehab and 3Department of Anterograde tracing studies revealed more 2Physical Med & Rehab and 3Department of Anterograde tracing studies revealed more 2Physical Med & Rehab and 3Department of Anterograde tracing studies revealed more Biomedical Engineering, Cleveland Clinic regenerated fibers in the distal end of the spinal Biomedical Engineering, Cleveland Clinic regenerated fibers in the distal end of the spinal Biomedical Engineering, Cleveland Clinic regenerated fibers in the distal end of the spinal

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 49 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 49 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 49 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE cord in the ST+PNG+aFGF+ChABC group. Behavioral assessment of bladder function was cord in the ST+PNG+aFGF+ChABC group. Behavioral assessment of bladder function was cord in the ST+PNG+aFGF+ChABC group. Behavioral assessment of bladder function was The improvements in bladder reflexes might recorded by daily manual bladder expression The improvements in bladder reflexes might recorded by daily manual bladder expression The improvements in bladder reflexes might recorded by daily manual bladder expression have been due to newly formed supraspinal and measurement of retained urine. Naïve have been due to newly formed supraspinal and measurement of retained urine. Naïve have been due to newly formed supraspinal and measurement of retained urine. Naïve control via nerve regeneration. animals demonstrated normal LUT behavior and control via nerve regeneration. animals demonstrated normal LUT behavior and control via nerve regeneration. animals demonstrated normal LUT behavior and electrophysiology. Unilateral injury animals electrophysiology. Unilateral injury animals electrophysiology. Unilateral injury animals P-26 Early and late behavioral and demonstrated normal LUT behavior throughout, P-26 Early and late behavioral and demonstrated normal LUT behavior throughout, P-26 Early and late behavioral and demonstrated normal LUT behavior throughout, electrophysiological changes in lower urinary and normal electrophysiology at early time- electrophysiological changes in lower urinary and normal electrophysiology at early time- electrophysiological changes in lower urinary and normal electrophysiology at early time- tract function following mid-cervical spinal points (post-injury days 7, 14), but abnormal tract function following mid-cervical spinal points (post-injury days 7, 14), but abnormal tract function following mid-cervical spinal points (post-injury days 7, 14), but abnormal cord injury electrophysiology at late time-points (post- cord injury electrophysiology at late time-points (post- cord injury electrophysiology at late time-points (post- injury days 28, 56). Bilateral injury animals injury days 28, 56). Bilateral injury animals injury days 28, 56). Bilateral injury animals T. Martin – Carreras1, G. Grossl1, D.D. Fuller3, demonstrated significant early LUT behavior T. Martin – Carreras1, G. Grossl1, D.D. Fuller3, demonstrated significant early LUT behavior T. Martin – Carreras1, G. Grossl1, D.D. Fuller3, demonstrated significant early LUT behavior P.J Reier2, M.A. Lane2, D.J. Hoh1,2 dysfunction (<14 days post-injury) and P.J Reier2, M.A. Lane2, D.J. Hoh1,2 dysfunction (<14 days post-injury) and P.J Reier2, M.A. Lane2, D.J. Hoh1,2 dysfunction (<14 days post-injury) and Department of Neurosurgery1 and concomitant abnormal electrophysiology (post- Department of Neurosurgery1 and concomitant abnormal electrophysiology (post- Department of Neurosurgery1 and concomitant abnormal electrophysiology (post- Department of Neuroscience2, College of injury days 7, 14). After 14 days, bilateral Department of Neuroscience2, College of injury days 7, 14). After 14 days, bilateral Department of Neuroscience2, College of injury days 7, 14). After 14 days, bilateral Medicine and McKnight Brain Institute; injury animals recovered normal LUT behavior, Medicine and McKnight Brain Institute; injury animals recovered normal LUT behavior, Medicine and McKnight Brain Institute; injury animals recovered normal LUT behavior, Department of Physical Therapy3, College of but had persistent late abnormal Department of Physical Therapy3, College of but had persistent late abnormal Department of Physical Therapy3, College of but had persistent late abnormal Public Health and Health Professions, electrophysiology (post-injury days 28, 56). Public Health and Health Professions, electrophysiology (post-injury days 28, 56). Public Health and Health Professions, electrophysiology (post-injury days 28, 56). University of Florida, Gainesville, FL Therefore, with this novel preclinical model, we University of Florida, Gainesville, FL Therefore, with this novel preclinical model, we University of Florida, Gainesville, FL Therefore, with this novel preclinical model, we demonstrate that despite recovery of LUT demonstrate that despite recovery of LUT demonstrate that despite recovery of LUT Lower urinary tract (LUT) dysfunction function behaviorally, abnormal changes Lower urinary tract (LUT) dysfunction function behaviorally, abnormal changes Lower urinary tract (LUT) dysfunction function behaviorally, abnormal changes is often a significant source of morbidity after electrophysiologically in LUT function are is often a significant source of morbidity after electrophysiologically in LUT function are is often a significant source of morbidity after electrophysiologically in LUT function are chronic spinal cord injury (SCI), irrespective of evident late after unilateral and bilateral cervical chronic spinal cord injury (SCI), irrespective of evident late after unilateral and bilateral cervical chronic spinal cord injury (SCI), irrespective of evident late after unilateral and bilateral cervical the spinal level involved. The majority of contusion injury, closely mirroring the clinical the spinal level involved. The majority of contusion injury, closely mirroring the clinical the spinal level involved. The majority of contusion injury, closely mirroring the clinical experimental studies of post-SCI LUT function, condition. experimental studies of post-SCI LUT function, condition. experimental studies of post-SCI LUT function, condition. however, have investigated only thoracic injury however, have investigated only thoracic injury however, have investigated only thoracic injury models, and have paradoxically shown recovery P-27 Integration of Microchannel Neural- models, and have paradoxically shown recovery P-27 Integration of Microchannel Neural- models, and have paradoxically shown recovery P-27 Integration of Microchannel Neural- of normal LUT function behaviorally after Electrode Interfaces Into Dorsal And Ventral of normal LUT function behaviorally after Electrode Interfaces Into Dorsal And Ventral of normal LUT function behaviorally after Electrode Interfaces Into Dorsal And Ventral injury. Few studies have shown abnormal LUT Roots For Bladder Control After Spinal Cord injury. Few studies have shown abnormal LUT Roots For Bladder Control After Spinal Cord injury. Few studies have shown abnormal LUT Roots For Bladder Control After Spinal Cord function electrophysiologically similar to that Injury function electrophysiologically similar to that Injury function electrophysiologically similar to that Injury seen clinically, characterized by bladder- seen clinically, characterized by bladder- seen clinically, characterized by bladder- external urethral sphincter (EUS) dyssynergy, D Chew1, E Delivopoulos2, N Granger3, S external urethral sphincter (EUS) dyssynergy, D Chew1, E Delivopoulos2, N Granger3, S external urethral sphincter (EUS) dyssynergy, D Chew1, E Delivopoulos2, N Granger3, S but only in thoracic injury models. Therefore, Mosse4, I Minev2, L Zhu8, S McMahon8, M but only in thoracic injury models. Therefore, Mosse4, I Minev2, L Zhu8, S McMahon8, M but only in thoracic injury models. Therefore, Mosse4, I Minev2, L Zhu8, S McMahon8, M we propose a study that to the best of our Craggs5, N Jeffery6, N Donaldson5, S Lacour7, J we propose a study that to the best of our Craggs5, N Jeffery6, N Donaldson5, S Lacour7, J we propose a study that to the best of our Craggs5, N Jeffery6, N Donaldson5, S Lacour7, J knowledge is the first of its kind, by examining Fawcett1 knowledge is the first of its kind, by examining Fawcett1 knowledge is the first of its kind, by examining Fawcett1 both early and late behavioral and 1Cambridge Centre for Brain Repair, both early and late behavioral and 1Cambridge Centre for Brain Repair, both early and late behavioral and 1Cambridge Centre for Brain Repair, electrophysiological changes in LUT function Department of Clinical Neuroscience, electrophysiological changes in LUT function Department of Clinical Neuroscience, electrophysiological changes in LUT function Department of Clinical Neuroscience, after experimental cervical contusion injury. University of Cambridge, Cambridge, UK; after experimental cervical contusion injury. University of Cambridge, Cambridge, UK; after experimental cervical contusion injury. University of Cambridge, Cambridge, UK; Mid-cervical (C4-5) unilateral (n=24) or 2Cambridge Nanoscience Centre, Department of Mid-cervical (C4-5) unilateral (n=24) or 2Cambridge Nanoscience Centre, Department of Mid-cervical (C4-5) unilateral (n=24) or 2Cambridge Nanoscience Centre, Department of bilateral (n=24) contusion injuries were Engineering, University of Cambridge, bilateral (n=24) contusion injuries were Engineering, University of Cambridge, bilateral (n=24) contusion injuries were Engineering, University of Cambridge, produced in adult Sprague–Dawley rats using Cambridge, UK; 3The Queen’s Veterinary produced in adult Sprague–Dawley rats using Cambridge, UK; 3The Queen’s Veterinary produced in adult Sprague–Dawley rats using Cambridge, UK; 3The Queen’s Veterinary the Infinite Horizon Impactor. Six naïve rats School Hospital, Department of Veterinary the Infinite Horizon Impactor. Six naïve rats School Hospital, Department of Veterinary the Infinite Horizon Impactor. Six naïve rats School Hospital, Department of Veterinary served as controls. LUT function was evaluated Medicine, University of Cambridge, Cambridge, served as controls. LUT function was evaluated Medicine, University of Cambridge, Cambridge, served as controls. LUT function was evaluated Medicine, University of Cambridge, Cambridge, electrophysiologically in all rats via continuous UK; 4Implanted Devices Group, Department of electrophysiologically in all rats via continuous UK; 4Implanted Devices Group, Department of electrophysiologically in all rats via continuous UK; 4Implanted Devices Group, Department of transurethral cystometry (7.5 ml/hr) and EUS Medical Physics, University College, London, transurethral cystometry (7.5 ml/hr) and EUS Medical Physics, University College, London, transurethral cystometry (7.5 ml/hr) and EUS Medical Physics, University College, London, electromyography. SCI animals were assessed UK; 5 Division of Surgery and Interventional electromyography. SCI animals were assessed UK; 5 Division of Surgery and Interventional electromyography. SCI animals were assessed UK; 5 Division of Surgery and Interventional on post-injury days 7, 14, 28, and 56. Science and Spinal Research Centre, RNOH, on post-injury days 7, 14, 28, and 56. Science and Spinal Research Centre, RNOH, on post-injury days 7, 14, 28, and 56. Science and Spinal Research Centre, RNOH,

50 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 50 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 50 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

Stanmore, London, UK; 6Department of implantation show that DRR is inappropriate for Stanmore, London, UK; 6Department of implantation show that DRR is inappropriate for Stanmore, London, UK; 6Department of implantation show that DRR is inappropriate for Veterinary Clinical Sciences, Iowa State the implantation procedure, with respect to axon Veterinary Clinical Sciences, Iowa State the implantation procedure, with respect to axon Veterinary Clinical Sciences, Iowa State the implantation procedure, with respect to axon University, Iowa, USA; 7 Laboratory for Soft survival and bladder morphology. At twelve University, Iowa, USA; 7 Laboratory for Soft survival and bladder morphology. At twelve University, Iowa, USA; 7 Laboratory for Soft survival and bladder morphology. At twelve Bioelectronic Interfaces, EPFL, Lausanne, weeks activity does return, suggestive of a Bioelectronic Interfaces, EPFL, Lausanne, weeks activity does return, suggestive of a Bioelectronic Interfaces, EPFL, Lausanne, weeks activity does return, suggestive of a Switzerland; 8Neurorestoration Group, Wolfson regenerative response, providing prospect for Switzerland; 8Neurorestoration Group, Wolfson regenerative response, providing prospect for Switzerland; 8Neurorestoration Group, Wolfson regenerative response, providing prospect for CARD, King’s College London, London, UK. ‘regenerative’ prosthetic design. The optimum CARD, King’s College London, London, UK. ‘regenerative’ prosthetic design. The optimum CARD, King’s College London, London, UK. ‘regenerative’ prosthetic design. The optimum scenario however, is keeping root-spinal cord scenario however, is keeping root-spinal cord scenario however, is keeping root-spinal cord A debilitating consequence of spinal continuity, with axon viability and bladder A debilitating consequence of spinal continuity, with axon viability and bladder A debilitating consequence of spinal continuity, with axon viability and bladder cord injury (SCI) is loss of bladder fullness morphology greatly improved. cord injury (SCI) is loss of bladder fullness morphology greatly improved. cord injury (SCI) is loss of bladder fullness morphology greatly improved. perception and micturition. The development of perception and micturition. The development of perception and micturition. The development of a hyper-reflexive bladder provides some relief P-28 Optimized acellular Grafts Support a hyper-reflexive bladder provides some relief P-28 Optimized acellular Grafts Support a hyper-reflexive bladder provides some relief P-28 Optimized acellular Grafts Support of urine. However, the dyssynergia between Functional Recovery after Cervical Spinal of urine. However, the dyssynergia between Functional Recovery after Cervical Spinal of urine. However, the dyssynergia between Functional Recovery after Cervical Spinal detrusor and sphincter results in incomplete Cord Injury detrusor and sphincter results in incomplete Cord Injury detrusor and sphincter results in incomplete Cord Injury expression and potential infection. An effective expression and potential infection. An effective expression and potential infection. An effective way to restore self-directed micturition is Z Z Khaing1, W J Alilain2, J Silver2, and C E way to restore self-directed micturition is Z Z Khaing1, W J Alilain2, J Silver2, and C E way to restore self-directed micturition is Z Z Khaing1, W J Alilain2, J Silver2, and C E artificially, through implantation of a Sacral Schmidt1 artificially, through implantation of a Sacral Schmidt1 artificially, through implantation of a Sacral Schmidt1 Anterior Root Stimulator (SARS). The critical 1 Department of Biomedical Anterior Root Stimulator (SARS). The critical 1 Department of Biomedical Anterior Root Stimulator (SARS). The critical 1 Department of Biomedical limitation is the inability to detect bladder Engineering, University of Texas at Austin, limitation is the inability to detect bladder Engineering, University of Texas at Austin, limitation is the inability to detect bladder Engineering, University of Texas at Austin, fullness, and therefore, when expression is Austin, Texas; 2 Department of Neurosciences, fullness, and therefore, when expression is Austin, Texas; 2 Department of Neurosciences, fullness, and therefore, when expression is Austin, Texas; 2 Department of Neurosciences, required. The project aims to use afferent Case Western Reserve University, Cleveland, required. The project aims to use afferent Case Western Reserve University, Cleveland, required. The project aims to use afferent Case Western Reserve University, Cleveland, information during bladder filling, to drive Ohio information during bladder filling, to drive Ohio information during bladder filling, to drive Ohio SARS output. This is to be accomplished SARS output. This is to be accomplished SARS output. This is to be accomplished through the design and implantation of Peripheral nerve (PN) grafts have been through the design and implantation of Peripheral nerve (PN) grafts have been through the design and implantation of Peripheral nerve (PN) grafts have been recording electrodes contained within used successfully as a bridge to support severed recording electrodes contained within used successfully as a bridge to support severed recording electrodes contained within used successfully as a bridge to support severed microchannels, onto the dorsal roots of rats. axons of the central nervous system (CNS) since microchannels, onto the dorsal roots of rats. axons of the central nervous system (CNS) since microchannels, onto the dorsal roots of rats. axons of the central nervous system (CNS) since When optimised, these prostheses will provide the early 80’s. However, the fresh PN grafts are When optimised, these prostheses will provide the early 80’s. However, the fresh PN grafts are When optimised, these prostheses will provide the early 80’s. However, the fresh PN grafts are indication for timely bladder expression in dogs not ideal for clinical translation because of indication for timely bladder expression in dogs not ideal for clinical translation because of indication for timely bladder expression in dogs not ideal for clinical translation because of suffering SCI, with the ultimate goal of limited availability, loss of function at the donor suffering SCI, with the ultimate goal of limited availability, loss of function at the donor suffering SCI, with the ultimate goal of limited availability, loss of function at the donor translation to humans. To date a newly designed site, and the need for multiple surgeries. translation to humans. To date a newly designed site, and the need for multiple surgeries. translation to humans. To date a newly designed site, and the need for multiple surgeries. SARS book electrode for the bilateral S2 ventral Recently, Dr. Schmidt’s group has developed an SARS book electrode for the bilateral S2 ventral Recently, Dr. Schmidt’s group has developed an SARS book electrode for the bilateral S2 ventral Recently, Dr. Schmidt’s group has developed an roots has been implanted successfully, with optimized acellular (OA) graft from peripheral roots has been implanted successfully, with optimized acellular (OA) graft from peripheral roots has been implanted successfully, with optimized acellular (OA) graft from peripheral maintained efficacy, in six dogs with SCI. Work nerve. This decellularization technique is now maintained efficacy, in six dogs with SCI. Work nerve. This decellularization technique is now maintained efficacy, in six dogs with SCI. Work nerve. This decellularization technique is now has focussed on identifying bladder afferent used produce acellular grafts from cadaver has focussed on identifying bladder afferent used produce acellular grafts from cadaver has focussed on identifying bladder afferent used produce acellular grafts from cadaver activity at acute and chronic implantation nerve tissue for clinical use in peripheral nerve activity at acute and chronic implantation nerve tissue for clinical use in peripheral nerve activity at acute and chronic implantation nerve tissue for clinical use in peripheral nerve stages, as well as optimising device design in repair. The acellular grafts were shown to be stages, as well as optimising device design in repair. The acellular grafts were shown to be stages, as well as optimising device design in repair. The acellular grafts were shown to be rat. We have electrophysiologically identified non-immunogenic and to support axonal growth rat. We have electrophysiologically identified non-immunogenic and to support axonal growth rat. We have electrophysiologically identified non-immunogenic and to support axonal growth bladder afferents during artificial bladder of severed axons after a complete thoracic cord bladder afferents during artificial bladder of severed axons after a complete thoracic cord bladder afferents during artificial bladder of severed axons after a complete thoracic cord infusion using a variety of microchannel injury in rodents. Here, we compared acellular infusion using a variety of microchannel injury in rodents. Here, we compared acellular infusion using a variety of microchannel injury in rodents. Here, we compared acellular devices. Bladder afferent action potentials are grafts to PN grafts in their ability to support devices. Bladder afferent action potentials are grafts to PN grafts in their ability to support devices. Bladder afferent action potentials are grafts to PN grafts in their ability to support small in amplitude compared to cutaneous and axonal growth in combination with small in amplitude compared to cutaneous and axonal growth in combination with small in amplitude compared to cutaneous and axonal growth in combination with muscle spindle, so the root must be ‘teased’ into chondroitnase ABC enzyme after cervical muscle spindle, so the root must be ‘teased’ into chondroitnase ABC enzyme after cervical muscle spindle, so the root must be ‘teased’ into chondroitnase ABC enzyme after cervical fascicules and insulated within 100 µm C3/C4 lateral hemisection injury. We assessed fascicules and insulated within 100 µm C3/C4 lateral hemisection injury. We assessed fascicules and insulated within 100 µm C3/C4 lateral hemisection injury. We assessed microchannels to improve the signal output. forelimb function of the animals using a microchannels to improve the signal output. forelimb function of the animals using a microchannels to improve the signal output. forelimb function of the animals using a Implants containing electrodes are fabricated cylinder paw preference test pre-surgery and bi- Implants containing electrodes are fabricated cylinder paw preference test pre-surgery and bi- Implants containing electrodes are fabricated cylinder paw preference test pre-surgery and bi- from polydimethylsiloxane (PDMS). Results weekly thereafter for up to 22 weeks post injury. from polydimethylsiloxane (PDMS). Results weekly thereafter for up to 22 weeks post injury. from polydimethylsiloxane (PDMS). Results weekly thereafter for up to 22 weeks post injury. after four weeks of L6/S1 dorsal root We found that immediately after injury, animals after four weeks of L6/S1 dorsal root We found that immediately after injury, animals after four weeks of L6/S1 dorsal root We found that immediately after injury, animals

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 51 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 51 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 51 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE in all groups lost the ability to explore with the reorganization of the hippocampal circuitry in in all groups lost the ability to explore with the reorganization of the hippocampal circuitry in in all groups lost the ability to explore with the reorganization of the hippocampal circuitry in affected limb during vertical exploration. In adult mice subjected to TBI, which was affected limb during vertical exploration. In adult mice subjected to TBI, which was affected limb during vertical exploration. In adult mice subjected to TBI, which was addition, we observed similar recovery profiles produced by a controlled cortical impact (CCI) addition, we observed similar recovery profiles produced by a controlled cortical impact (CCI) addition, we observed similar recovery profiles produced by a controlled cortical impact (CCI) for animals with PN and OA grafts. At 22 to the cortex above the hippocampus. BrdU was for animals with PN and OA grafts. At 22 to the cortex above the hippocampus. BrdU was for animals with PN and OA grafts. At 22 to the cortex above the hippocampus. BrdU was weeks, we resected the grafts and saw loss of injected daily from four to seven days after CCI weeks, we resected the grafts and saw loss of injected daily from four to seven days after CCI weeks, we resected the grafts and saw loss of injected daily from four to seven days after CCI forelimb function for PN and OA grafts, 65% or sham surgery, then mice were transferred to forelimb function for PN and OA grafts, 65% or sham surgery, then mice were transferred to forelimb function for PN and OA grafts, 65% or sham surgery, then mice were transferred to and 36% respectively. Anatomical track tracing either the institution standard cages (STD) or to and 36% respectively. Anatomical track tracing either the institution standard cages (STD) or to and 36% respectively. Anatomical track tracing either the institution standard cages (STD) or to and histological studies are underway to the EE. Four weeks later, mice were injected and histological studies are underway to the EE. Four weeks later, mice were injected and histological studies are underway to the EE. Four weeks later, mice were injected determine origin and extent of axonal growth with pseudorabies virus (PRV), a retrograde determine origin and extent of axonal growth with pseudorabies virus (PRV), a retrograde determine origin and extent of axonal growth with pseudorabies virus (PRV), a retrograde into and out of the grafts. Our results indicate, transynaptic neuronal tracer, into the entorhrinal into and out of the grafts. Our results indicate, transynaptic neuronal tracer, into the entorhrinal into and out of the grafts. Our results indicate, transynaptic neuronal tracer, into the entorhrinal for the first time, that acellular grafts can cortex, and euthanized 50 hours after the for the first time, that acellular grafts can cortex, and euthanized 50 hours after the for the first time, that acellular grafts can cortex, and euthanized 50 hours after the support CNS axon growth and support injection. Quantitative analysis was performed support CNS axon growth and support injection. Quantitative analysis was performed support CNS axon growth and support injection. Quantitative analysis was performed functional recovery to a similar extent to that of to estimate the number of retrogradely infected functional recovery to a similar extent to that of to estimate the number of retrogradely infected functional recovery to a similar extent to that of to estimate the number of retrogradely infected fresh PN. Our findings support the idea that cells by the PRV in the hippocampus ipsilateral fresh PN. Our findings support the idea that cells by the PRV in the hippocampus ipsilateral fresh PN. Our findings support the idea that cells by the PRV in the hippocampus ipsilateral acellular grafts can potentially serve as a to CCI. We found that the brain regions infected acellular grafts can potentially serve as a to CCI. We found that the brain regions infected acellular grafts can potentially serve as a to CCI. We found that the brain regions infected clinically relevant option for repair therapies by PRV were similar between the mice that clinically relevant option for repair therapies by PRV were similar between the mice that clinically relevant option for repair therapies by PRV were similar between the mice that after spinal cord injury. underwent sham surgery and CCI, suggesting a after spinal cord injury. underwent sham surgery and CCI, suggesting a after spinal cord injury. underwent sham surgery and CCI, suggesting a Support: this work was supported by the Gillson preservation of circuitry connected to the Support: this work was supported by the Gillson preservation of circuitry connected to the Support: this work was supported by the Gillson preservation of circuitry connected to the Longenbough Foundation (CES) and the David entorhrinal cortex and within the hippocampal Longenbough Foundation (CES) and the David entorhrinal cortex and within the hippocampal Longenbough Foundation (CES) and the David entorhrinal cortex and within the hippocampal Van Wagner Foundation (CES). trisynaptic circuit following TBI. When the Van Wagner Foundation (CES). trisynaptic circuit following TBI. When the Van Wagner Foundation (CES). trisynaptic circuit following TBI. When the third order of infection in the dentate gyrus third order of infection in the dentate gyrus third order of infection in the dentate gyrus P-29 Environmental Enrichment Enhances (DG) was corrected by the counts in the second P-29 Environmental Enrichment Enhances (DG) was corrected by the counts in the second P-29 Environmental Enrichment Enhances (DG) was corrected by the counts in the second Retrograde Transport of Polysynaptic Virus and first orders (DG/CA3/CA1), TBI-EE mice Retrograde Transport of Polysynaptic Virus and first orders (DG/CA3/CA1), TBI-EE mice Retrograde Transport of Polysynaptic Virus and first orders (DG/CA3/CA1), TBI-EE mice In The Dentate Gyrus After Traumatic Brain displayed a higher ratio of PRV infectivity In The Dentate Gyrus After Traumatic Brain displayed a higher ratio of PRV infectivity In The Dentate Gyrus After Traumatic Brain displayed a higher ratio of PRV infectivity Injury compared to that of TBI-STD mice (p=0.065) Injury compared to that of TBI-STD mice (p=0.065) Injury compared to that of TBI-STD mice (p=0.065) and EE produced a higher ratio overall (p<0.05). and EE produced a higher ratio overall (p<0.05). and EE produced a higher ratio overall (p<0.05). C. Burger1,2, R. Zamanskaya1,2, 3, W. Liu1,2, T.-J. BrdU data suggest more neurogenesis not only C. Burger1,2, R. Zamanskaya1,2, 3, W. Liu1,2, T.-J. BrdU data suggest more neurogenesis not only C. Burger1,2, R. Zamanskaya1,2, 3, W. Liu1,2, T.-J. BrdU data suggest more neurogenesis not only Chang1,2, *J. Liu1,2; in animals exposed to EE compared to STD Chang1,2, *J. Liu1,2; in animals exposed to EE compared to STD Chang1,2, *J. Liu1,2; in animals exposed to EE compared to STD Dept. of Neurological Surgery, conditions (p<0.001), but also in those subjected Dept. of Neurological Surgery, conditions (p<0.001), but also in those subjected Dept. of Neurological Surgery, conditions (p<0.001), but also in those subjected University of California1, and SFVAMC2, San to TBI than sham (p<0.01). The degree to University of California1, and SFVAMC2, San to TBI than sham (p<0.01). The degree to University of California1, and SFVAMC2, San to TBI than sham (p<0.01). The degree to Francisco, CA; 3University of California, Davis, which EE-induced DG neurogenesis affects Francisco, CA; 3University of California, Davis, which EE-induced DG neurogenesis affects Francisco, CA; 3University of California, Davis, which EE-induced DG neurogenesis affects CA transneuronal spread of virus is under further CA transneuronal spread of virus is under further CA transneuronal spread of virus is under further investigation. investigation. investigation. One of the long-term neurological One of the long-term neurological One of the long-term neurological sequelae associated with traumatic brain injury P-30 Analysis of Gene Expression sequelae associated with traumatic brain injury P-30 Analysis of Gene Expression sequelae associated with traumatic brain injury P-30 Analysis of Gene Expression (TBI) is memory dysfunction. TBI is also one of Following A Localized Traumatic Brain (TBI) is memory dysfunction. TBI is also one of Following A Localized Traumatic Brain (TBI) is memory dysfunction. TBI is also one of Following A Localized Traumatic Brain the most potent risk factors for development of Injury Reveals A Bias Toward Increased Cell the most potent risk factors for development of Injury Reveals A Bias Toward Increased Cell the most potent risk factors for development of Injury Reveals A Bias Toward Increased Cell neurodegeneration. Enriched environment (EE) Death Locally And Cell Survival Remotely neurodegeneration. Enriched environment (EE) Death Locally And Cell Survival Remotely neurodegeneration. Enriched environment (EE) Death Locally And Cell Survival Remotely is known to improve function in experimental is known to improve function in experimental is known to improve function in experimental models of TBI. Although EE-elicited T. E. White1, G. D. Ford1, A. Gates1, M. models of TBI. Although EE-elicited T. E. White1, G. D. Ford1, A. Gates1, M. models of TBI. Although EE-elicited T. E. White1, G. D. Ford1, A. Gates1, M. hippocampal neurogenesis has been well LaPlaca2, B. D. Ford1 hippocampal neurogenesis has been well LaPlaca2, B. D. Ford1 hippocampal neurogenesis has been well LaPlaca2, B. D. Ford1 documented after TBI, EE-induced synaptic 1Department of Neurobiology, documented after TBI, EE-induced synaptic 1Department of Neurobiology, documented after TBI, EE-induced synaptic 1Department of Neurobiology, reorganization that might underlie the observed Neuroscience Institute, Morehouse School of reorganization that might underlie the observed Neuroscience Institute, Morehouse School of reorganization that might underlie the observed Neuroscience Institute, Morehouse School of benefit in functional memory has not been Medicine, Atlanta, GA, USA; 2Department of benefit in functional memory has not been Medicine, Atlanta, GA, USA; 2Department of benefit in functional memory has not been Medicine, Atlanta, GA, USA; 2Department of explored. The current study sought to determine Biomedical Engineering, Georgia Institute of explored. The current study sought to determine Biomedical Engineering, Georgia Institute of explored. The current study sought to determine Biomedical Engineering, Georgia Institute of whether exposure to EE induced synaptic Technology, Atlanta, GA, USA whether exposure to EE induced synaptic Technology, Atlanta, GA, USA whether exposure to EE induced synaptic Technology, Atlanta, GA, USA

52 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 52 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 52 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

We used microarray and bioinformatic This work was supported by NIH grant R01 We used microarray and bioinformatic This work was supported by NIH grant R01 We used microarray and bioinformatic This work was supported by NIH grant R01 analysis to better understand how gene NS056446-04 analysis to better understand how gene NS056446-04 analysis to better understand how gene NS056446-04 expression is modulated throughout the brain by expression is modulated throughout the brain by expression is modulated throughout the brain by localized traumatic brain injury (TBI). Adult P-31 Training of The Impaired Forelimb localized traumatic brain injury (TBI). Adult P-31 Training of The Impaired Forelimb localized traumatic brain injury (TBI). Adult P-31 Training of The Impaired Forelimb Sprague-Dawley rats received unilateral After Traumatic Brain Injury Enhances Sprague-Dawley rats received unilateral After Traumatic Brain Injury Enhances Sprague-Dawley rats received unilateral After Traumatic Brain Injury Enhances controlled cortical impacts and were sacrificed Hippocampal Neurogenesis In Mice Without controlled cortical impacts and were sacrificed Hippocampal Neurogenesis In Mice Without controlled cortical impacts and were sacrificed Hippocampal Neurogenesis In Mice Without 24 hours post-injury. mRNAs isolated from the Corpus Callosum 24 hours post-injury. mRNAs isolated from the Corpus Callosum 24 hours post-injury. mRNAs isolated from the Corpus Callosum brain tissues of these rats and naïve (control) brain tissues of these rats and naïve (control) brain tissues of these rats and naïve (control) rats were hybridized to the Affymetrix Rat S. Wu1, 3, M. Neumann1, 3, W. Liu1, 3, C.C. Lee1, 3, rats were hybridized to the Affymetrix Rat S. Wu1, 3, M. Neumann1, 3, W. Liu1, 3, C.C. Lee1, 3, rats were hybridized to the Affymetrix Rat S. Wu1, 3, M. Neumann1, 3, W. Liu1, 3, C.C. Lee1, 3, Genome 230 2.0 GeneChip for microarray R. Zamanskaya1, 3, L. Noble-Haeusslein1, 2 and Genome 230 2.0 GeneChip for microarray R. Zamanskaya1, 3, L. Noble-Haeusslein1, 2 and Genome 230 2.0 GeneChip for microarray R. Zamanskaya1, 3, L. Noble-Haeusslein1, 2 and analysis. We identified genes that changed in J. Liu1, 3 analysis. We identified genes that changed in J. Liu1, 3 analysis. We identified genes that changed in J. Liu1, 3 expression by 2-fold or more on both the Departments of Neurological Surgery1 expression by 2-fold or more on both the Departments of Neurological Surgery1 expression by 2-fold or more on both the Departments of Neurological Surgery1 ipsilateral and contralateral sides of the brain. and Physical Therapy and Rehabilitation ipsilateral and contralateral sides of the brain. and Physical Therapy and Rehabilitation ipsilateral and contralateral sides of the brain. and Physical Therapy and Rehabilitation Ingenuity Pathway Analysis was used to Science2, UCSF and SFVAMC3, San Francisco, Ingenuity Pathway Analysis was used to Science2, UCSF and SFVAMC3, San Francisco, Ingenuity Pathway Analysis was used to Science2, UCSF and SFVAMC3, San Francisco, identify the functions, canonical pathways, and California identify the functions, canonical pathways, and California identify the functions, canonical pathways, and California networks most significant to the data set. Cell networks most significant to the data set. Cell networks most significant to the data set. Cell death was the most significant functional The corpus callosum, as the principal death was the most significant functional The corpus callosum, as the principal death was the most significant functional The corpus callosum, as the principal category common to both sides of the brain. fiber tract interconnecting the left and right category common to both sides of the brain. fiber tract interconnecting the left and right category common to both sides of the brain. fiber tract interconnecting the left and right Ipsilaterally, 90% of the 272 unique (unchanged cortices, mediates interhemispheric crosstalk Ipsilaterally, 90% of the 272 unique (unchanged cortices, mediates interhemispheric crosstalk Ipsilaterally, 90% of the 272 unique (unchanged cortices, mediates interhemispheric crosstalk on the opposite side) cell death genes that and spatial coupling between the limbs. on the opposite side) cell death genes that and spatial coupling between the limbs. on the opposite side) cell death genes that and spatial coupling between the limbs. changed in expression showed increased Unilateral brain injury, such as stroke, is known changed in expression showed increased Unilateral brain injury, such as stroke, is known changed in expression showed increased Unilateral brain injury, such as stroke, is known expression; including known apoptotic factors, to disrupt the balance between the two cortices expression; including known apoptotic factors, to disrupt the balance between the two cortices expression; including known apoptotic factors, to disrupt the balance between the two cortices caspases 3, 4, and 7, cyclooxygenase, and as evidenced by an abnormally high caspases 3, 4, and 7, cyclooxygenase, and as evidenced by an abnormally high caspases 3, 4, and 7, cyclooxygenase, and as evidenced by an abnormally high several members of the s100 family. Several key interhemispheric inhibitory drive from M1intact several members of the s100 family. Several key interhemispheric inhibitory drive from M1intact several members of the s100 family. Several key interhemispheric inhibitory drive from M1intact transcription factors also showed increased to M1lesioned transmitted transcallosally. Our transcription factors also showed increased to M1lesioned transmitted transcallosally. Our transcription factors also showed increased to M1lesioned transmitted transcallosally. Our expression; including FOS, MYC, CEBPB, previous work showed that the deletion of expression; including FOS, MYC, CEBPB, previous work showed that the deletion of expression; including FOS, MYC, CEBPB, previous work showed that the deletion of CREBBP, and NFKB2. Contralaterally, 77% of homeobox gene Emx1 not only led to the CREBBP, and NFKB2. Contralaterally, 77% of homeobox gene Emx1 not only led to the CREBBP, and NFKB2. Contralaterally, 77% of homeobox gene Emx1 not only led to the the 94 unique cell death genes decreased in agenesis of the corpus callosum but also the 94 unique cell death genes decreased in agenesis of the corpus callosum but also the 94 unique cell death genes decreased in agenesis of the corpus callosum but also expression; including cell death promoting reduced hippocampal neurogenesis. The current expression; including cell death promoting reduced hippocampal neurogenesis. The current expression; including cell death promoting reduced hippocampal neurogenesis. The current genes BAX and HSP90AA1 and the study sought to determine whether lacking the genes BAX and HSP90AA1 and the study sought to determine whether lacking the genes BAX and HSP90AA1 and the study sought to determine whether lacking the transcription factor SP1. Additionally, there are corpus callosum affected the recovery of transcription factor SP1. Additionally, there are corpus callosum affected the recovery of transcription factor SP1. Additionally, there are corpus callosum affected the recovery of 279 cell death genes that change on both sides forelimb function and hippocampal plasticity 279 cell death genes that change on both sides forelimb function and hippocampal plasticity 279 cell death genes that change on both sides forelimb function and hippocampal plasticity of the brain. 47 of these genes show differential following training of the affected limb in mice of the brain. 47 of these genes show differential following training of the affected limb in mice of the brain. 47 of these genes show differential following training of the affected limb in mice expression. Cyclin D1 and STAT3 increase with unilateral traumatic brain injury (TBI). One expression. Cyclin D1 and STAT3 increase with unilateral traumatic brain injury (TBI). One expression. Cyclin D1 and STAT3 increase with unilateral traumatic brain injury (TBI). One ipsilaterally and decrease contralaterally. While week after TBI, produced by a controlled ipsilaterally and decrease contralaterally. While week after TBI, produced by a controlled ipsilaterally and decrease contralaterally. While week after TBI, produced by a controlled CD44 expression increases on both sides, its cortical impact to impair the preferred limb, CD44 expression increases on both sides, its cortical impact to impair the preferred limb, CD44 expression increases on both sides, its cortical impact to impair the preferred limb, expression is 6.5 times higher on the ipsilateral Emx1 wild type (WT) and knock out (KO) mice expression is 6.5 times higher on the ipsilateral Emx1 wild type (WT) and knock out (KO) mice expression is 6.5 times higher on the ipsilateral Emx1 wild type (WT) and knock out (KO) mice side. The observed expression pattern for cell were subjected to the single-pellet reaching side. The observed expression pattern for cell were subjected to the single-pellet reaching side. The observed expression pattern for cell were subjected to the single-pellet reaching death genes suggests that cell death would be training task with the affected limb for a period death genes suggests that cell death would be training task with the affected limb for a period death genes suggests that cell death would be training task with the affected limb for a period more likely to occur ipsilaterally and less likely of 4 weeks. Over the training period, all groups more likely to occur ipsilaterally and less likely of 4 weeks. Over the training period, all groups more likely to occur ipsilaterally and less likely of 4 weeks. Over the training period, all groups to occur contralaterally. Extension of the improved on the task as evidenced by a to occur contralaterally. Extension of the improved on the task as evidenced by a to occur contralaterally. Extension of the improved on the task as evidenced by a bioinformatic analyses used in this experiment progressive increase in the successful rate in bioinformatic analyses used in this experiment progressive increase in the successful rate in bioinformatic analyses used in this experiment progressive increase in the successful rate in will be useful for identifying novel molecules reaching and grasping the pellet (p<0.0001). will be useful for identifying novel molecules reaching and grasping the pellet (p<0.0001). will be useful for identifying novel molecules reaching and grasping the pellet (p<0.0001). that may be targets for preventing TBI related Both TBI and Emx1 deletion had overall that may be targets for preventing TBI related Both TBI and Emx1 deletion had overall that may be targets for preventing TBI related Both TBI and Emx1 deletion had overall cell death. adverse effects on the performance of the cell death. adverse effects on the performance of the cell death. adverse effects on the performance of the reaching task (two-way repeated ANOVA: reaching task (two-way repeated ANOVA: reaching task (two-way repeated ANOVA:

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 53 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 53 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 53 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE p<0.01 and p<0.05, respectively), although functional outcome. Traumatic brain injury was p<0.01 and p<0.05, respectively), although functional outcome. Traumatic brain injury was p<0.01 and p<0.05, respectively), although functional outcome. Traumatic brain injury was Emx1 KO mice did not perform significantly induced by a controlled cortical impact (CCI) Emx1 KO mice did not perform significantly induced by a controlled cortical impact (CCI) Emx1 KO mice did not perform significantly induced by a controlled cortical impact (CCI) worse than their WT counterparts (post hoc: using the following parameters: 1.5 m/s strike worse than their WT counterparts (post hoc: using the following parameters: 1.5 m/s strike worse than their WT counterparts (post hoc: using the following parameters: 1.5 m/s strike p>0.16). Both TBI and Emx1 gene deletion also velocity, 2.5 mm depth of penetration and a p>0.16). Both TBI and Emx1 gene deletion also velocity, 2.5 mm depth of penetration and a p>0.16). Both TBI and Emx1 gene deletion also velocity, 2.5 mm depth of penetration and a had a strong effect on hippocampal dwell time of 120 msec. Botox was injected into had a strong effect on hippocampal dwell time of 120 msec. Botox was injected into had a strong effect on hippocampal dwell time of 120 msec. Botox was injected into neurogenesis (p<0.001 and p<0.0001, the unaffected forelimb immediately post CCI to neurogenesis (p<0.001 and p<0.0001, the unaffected forelimb immediately post CCI to neurogenesis (p<0.001 and p<0.0001, the unaffected forelimb immediately post CCI to respectively), demonstrated by a reduction in discourage the use of the unaffected limb. respectively), demonstrated by a reduction in discourage the use of the unaffected limb. respectively), demonstrated by a reduction in discourage the use of the unaffected limb. doublecortin (DCX)- expressing immature Minocycline administered via bolus i.p. at doublecortin (DCX)- expressing immature Minocycline administered via bolus i.p. at doublecortin (DCX)- expressing immature Minocycline administered via bolus i.p. at neurons, while limb training enhanced DCX 25mg/kg commenced at 24 hrs post injury for neurons, while limb training enhanced DCX 25mg/kg commenced at 24 hrs post injury for neurons, while limb training enhanced DCX 25mg/kg commenced at 24 hrs post injury for expression (p<0.005). Our results suggest that 12 consecutive days. A two-week physical expression (p<0.005). Our results suggest that 12 consecutive days. A two-week physical expression (p<0.005). Our results suggest that 12 consecutive days. A two-week physical lacking corpus callosum has a more pronounced therapy regimen consisting of daily exercise on lacking corpus callosum has a more pronounced therapy regimen consisting of daily exercise on lacking corpus callosum has a more pronounced therapy regimen consisting of daily exercise on impact on forelimb dexterity in uninjured mice ropes, grids and balls began at 5 days post TBI. impact on forelimb dexterity in uninjured mice ropes, grids and balls began at 5 days post TBI. impact on forelimb dexterity in uninjured mice ropes, grids and balls began at 5 days post TBI. as compared to those with TBI. Our findings All animals underwent behavioral evaluation 4 as compared to those with TBI. Our findings All animals underwent behavioral evaluation 4 as compared to those with TBI. Our findings All animals underwent behavioral evaluation 4 also suggest that limb training enhances weeks and 8 weeks post injury. TBI induced also suggest that limb training enhances weeks and 8 weeks post injury. TBI induced also suggest that limb training enhances weeks and 8 weeks post injury. TBI induced neuroplasticity after brain injury at functionally impairment not only in motor but also in neuroplasticity after brain injury at functionally impairment not only in motor but also in neuroplasticity after brain injury at functionally impairment not only in motor but also in remote regions, including the hippocampus, cognitive domains. Minocycline treatment led to remote regions, including the hippocampus, cognitive domains. Minocycline treatment led to remote regions, including the hippocampus, cognitive domains. Minocycline treatment led to which might have implications for promoting a significant reduction in activated microglia in which might have implications for promoting a significant reduction in activated microglia in which might have implications for promoting a significant reduction in activated microglia in overall recovery of function. the peri-lesional area, however no significant overall recovery of function. the peri-lesional area, however no significant overall recovery of function. the peri-lesional area, however no significant reduction in lesion volume. Rats treated with reduction in lesion volume. Rats treated with reduction in lesion volume. Rats treated with P-32 Using Multimodel Therapies To minocycline also appeared to perform P-32 Using Multimodel Therapies To minocycline also appeared to perform P-32 Using Multimodel Therapies To minocycline also appeared to perform Improve Outcome Following Traumatic significantly better in the sticky tape removal Improve Outcome Following Traumatic significantly better in the sticky tape removal Improve Outcome Following Traumatic significantly better in the sticky tape removal Brain Injury test and the Morris Water maze when compared Brain Injury test and the Morris Water maze when compared Brain Injury test and the Morris Water maze when compared to vehicle treated controls. The combination of to vehicle treated controls. The combination of to vehicle treated controls. The combination of D. Bingham1, T. Lam2, J. Lee1, T.J. Chang1, C. physical therapy and botox appeared to have no D. Bingham1, T. Lam2, J. Lee1, T.J. Chang1, C. physical therapy and botox appeared to have no D. Bingham1, T. Lam2, J. Lee1, T.J. Chang1, C. physical therapy and botox appeared to have no Burger1, C. Sun1, S. Wu1, J. Shi2, S. Massa2, R. beneficial effect on functional outcome, Burger1, C. Sun1, S. Wu1, J. Shi2, S. Massa2, R. beneficial effect on functional outcome, Burger1, C. Sun1, S. Wu1, J. Shi2, S. Massa2, R. beneficial effect on functional outcome, A. Swanson2, J. Liu1. possibly due to the confounding effect of botox A. Swanson2, J. Liu1. possibly due to the confounding effect of botox A. Swanson2, J. Liu1. possibly due to the confounding effect of botox Depts. of Neurosurgery1, and on the contralesional forelimb. Our results Depts. of Neurosurgery1, and on the contralesional forelimb. Our results Depts. of Neurosurgery1, and on the contralesional forelimb. Our results Neurology2; Veterans Affairs Medical Center suggest that delayed and chronic treatment with Neurology2; Veterans Affairs Medical Center suggest that delayed and chronic treatment with Neurology2; Veterans Affairs Medical Center suggest that delayed and chronic treatment with and University of California, San Francisco, minocycline can reduce inflammation and and University of California, San Francisco, minocycline can reduce inflammation and and University of California, San Francisco, minocycline can reduce inflammation and California 94121, USA. improve outcome following TBI. California 94121, USA. improve outcome following TBI. California 94121, USA. improve outcome following TBI.

Traumatic brain injury is one of the P-33 Stroke Affects Functional Activation Traumatic brain injury is one of the P-33 Stroke Affects Functional Activation Traumatic brain injury is one of the P-33 Stroke Affects Functional Activation leading causes of long-term disability in the During Spatial Tasks leading causes of long-term disability in the During Spatial Tasks leading causes of long-term disability in the During Spatial Tasks young adults in Western world. To date current young adults in Western world. To date current young adults in Western world. To date current treatment of TBI focuses primarily on S. Badurek1,2, W. Liu1,2, C. Burger1,2, C. Lee1,2, treatment of TBI focuses primarily on S. Badurek1,2, W. Liu1,2, C. Burger1,2, C. Lee1,2, treatment of TBI focuses primarily on S. Badurek1,2, W. Liu1,2, C. Burger1,2, C. Lee1,2, maintaining vital functions and reducing R. Saloner1,2, J. Liu1,2 maintaining vital functions and reducing R. Saloner1,2, J. Liu1,2 maintaining vital functions and reducing R. Saloner1,2, J. Liu1,2 intracranial pressure. Therefore, new efficacious Department of Neurological Surgery, intracranial pressure. Therefore, new efficacious Department of Neurological Surgery, intracranial pressure. Therefore, new efficacious Department of Neurological Surgery, treatments are essential that target both the UCSF1 and SFVAMC2, San Francisco, treatments are essential that target both the UCSF1 and SFVAMC2, San Francisco, treatments are essential that target both the UCSF1 and SFVAMC2, San Francisco, resulting physical and mental disabilities. California resulting physical and mental disabilities. California resulting physical and mental disabilities. California Constrain induced movement therapy (CIMT) Constrain induced movement therapy (CIMT) Constrain induced movement therapy (CIMT) has been shown to be efficacious in human Post-stroke impairment of short- and has been shown to be efficacious in human Post-stroke impairment of short- and has been shown to be efficacious in human Post-stroke impairment of short- and studies of stroke to improve physical recovery long-term memory is not uncommon, yet the studies of stroke to improve physical recovery long-term memory is not uncommon, yet the studies of stroke to improve physical recovery long-term memory is not uncommon, yet the as well as induce cortical remapping. We underlying mechanism is unclear. The as well as induce cortical remapping. We underlying mechanism is unclear. The as well as induce cortical remapping. We underlying mechanism is unclear. The proposed combining the CIMT with an anti- hippocampus is involved in memory function, proposed combining the CIMT with an anti- hippocampus is involved in memory function, proposed combining the CIMT with an anti- hippocampus is involved in memory function, inflammatory treatment to reduce the secondary but direct ischemic lesions strategic to the inflammatory treatment to reduce the secondary but direct ischemic lesions strategic to the inflammatory treatment to reduce the secondary but direct ischemic lesions strategic to the injury component of TBI as well as improve hippocampus/parahippocampus are rarely injury component of TBI as well as improve hippocampus/parahippocampus are rarely injury component of TBI as well as improve hippocampus/parahippocampus are rarely

54 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 54 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 54 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE observed in middle cerebral artery (MCA) C. Sun1, 2, H. Sun1, 2, S. Wu1, 2, T.J. Chang1,2, R. observed in middle cerebral artery (MCA) C. Sun1, 2, H. Sun1, 2, S. Wu1, 2, T.J. Chang1,2, R. observed in middle cerebral artery (MCA) C. Sun1, 2, H. Sun1, 2, S. Wu1, 2, T.J. Chang1,2, R. stroke. Previously, we found that stroke by Saloner1, 2, 3, S.G. Kernie4 and J. Liu1, 2 stroke. Previously, we found that stroke by Saloner1, 2, 3, S.G. Kernie4 and J. Liu1, 2 stroke. Previously, we found that stroke by Saloner1, 2, 3, S.G. Kernie4 and J. Liu1, 2 distal occlusion of MCA produced injury 1Department of Neurological Surgery, distal occlusion of MCA produced injury 1Department of Neurological Surgery, distal occlusion of MCA produced injury 1Department of Neurological Surgery, restricted to the parietal cortex and mild University of California, San Francisco, San restricted to the parietal cortex and mild University of California, San Francisco, San restricted to the parietal cortex and mild University of California, San Francisco, San memory impairment. It is well known that the Francisco, CA.; 2Department of Neurological memory impairment. It is well known that the Francisco, CA.; 2Department of Neurological memory impairment. It is well known that the Francisco, CA.; 2Department of Neurological interplay of several brain regions is crucial for Surgery, San Francisco Veteran Affairs Medical interplay of several brain regions is crucial for Surgery, San Francisco Veteran Affairs Medical interplay of several brain regions is crucial for Surgery, San Francisco Veteran Affairs Medical learning and memory. Recent advances also Center, San Francisco, CA.; 3University of learning and memory. Recent advances also Center, San Francisco, CA.; 3University of learning and memory. Recent advances also Center, San Francisco, CA.; 3University of suggest that shared neuronal activation patterns California, Davis, Davis, CA; 4Departments of suggest that shared neuronal activation patterns California, Davis, Davis, CA; 4Departments of suggest that shared neuronal activation patterns California, Davis, Davis, CA; 4Departments of define brain networks linking anatomically Pathology and Cell Biology, College of define brain networks linking anatomically Pathology and Cell Biology, College of define brain networks linking anatomically Pathology and Cell Biology, College of separate brain regions. Since the parietal cortex Physicians and Surgeons, Columbia University, separate brain regions. Since the parietal cortex Physicians and Surgeons, Columbia University, separate brain regions. Since the parietal cortex Physicians and Surgeons, Columbia University, receives highly processed spatial information, New York, NY. receives highly processed spatial information, New York, NY. receives highly processed spatial information, New York, NY. the present study sought to investigate how the present study sought to investigate how the present study sought to investigate how ischemic injury in the parietal cortex disrupted The causal relationship between ischemic injury in the parietal cortex disrupted The causal relationship between ischemic injury in the parietal cortex disrupted The causal relationship between multiple brain regions involved in spatial neurogenesis and post-stroke functional multiple brain regions involved in spatial neurogenesis and post-stroke functional multiple brain regions involved in spatial neurogenesis and post-stroke functional processing. Stroke was induced in rats by distal recovery has not been properly explored. The processing. Stroke was induced in rats by distal recovery has not been properly explored. The processing. Stroke was induced in rats by distal recovery has not been properly explored. The middle cerebral artery occlusion (dMCAO). current study aimed to determine whether middle cerebral artery occlusion (dMCAO). current study aimed to determine whether middle cerebral artery occlusion (dMCAO). current study aimed to determine whether Neuronal activation induced by spatial attenuation of neuroprogenitor cells affects the Neuronal activation induced by spatial attenuation of neuroprogenitor cells affects the Neuronal activation induced by spatial attenuation of neuroprogenitor cells affects the exploration was mapped by immediate early post-stroke functional outcome. Ischemic or exploration was mapped by immediate early post-stroke functional outcome. Ischemic or exploration was mapped by immediate early post-stroke functional outcome. Ischemic or gene Fos in the motor and limbic systems and in sham stroke was induced by distal medial gene Fos in the motor and limbic systems and in sham stroke was induced by distal medial gene Fos in the motor and limbic systems and in sham stroke was induced by distal medial the thalamic nuclei that receive input from cerebral artery occlusion (dMCAO) in 10-week- the thalamic nuclei that receive input from cerebral artery occlusion (dMCAO) in 10-week- the thalamic nuclei that receive input from cerebral artery occlusion (dMCAO) in 10-week- sensory systems. In awake animals during old nestin-δ-HSV-TK-eGFP transgenic mice, in sensory systems. In awake animals during old nestin-δ-HSV-TK-eGFP transgenic mice, in sensory systems. In awake animals during old nestin-δ-HSV-TK-eGFP transgenic mice, in resting state in home cages, regions such as the which expression of a truncated viral thymidine resting state in home cages, regions such as the which expression of a truncated viral thymidine resting state in home cages, regions such as the which expression of a truncated viral thymidine dentate gyrus were not silent, suggesting kinase gene and an eGFP gene was restricted to dentate gyrus were not silent, suggesting kinase gene and an eGFP gene was restricted to dentate gyrus were not silent, suggesting kinase gene and an eGFP gene was restricted to ongoing information processing. Contrary to type-1 neural progenitor cells, enabling both ongoing information processing. Contrary to type-1 neural progenitor cells, enabling both ongoing information processing. Contrary to type-1 neural progenitor cells, enabling both those that remained in home cages, rats conditional ablation by ganciclovir (GCV) and those that remained in home cages, rats conditional ablation by ganciclovir (GCV) and those that remained in home cages, rats conditional ablation by ganciclovir (GCV) and exploring a novel environment exhibited eGFP-tagging of these neuroprogenitor cells. exploring a novel environment exhibited eGFP-tagging of these neuroprogenitor cells. exploring a novel environment exhibited eGFP-tagging of these neuroprogenitor cells. activation of all regions examined. However, a GCV (200 mg/kg/day) or saline was activation of all regions examined. However, a GCV (200 mg/kg/day) or saline was activation of all regions examined. However, a GCV (200 mg/kg/day) or saline was region-specific reduction in neuronal activation continuously administered via osmotic pumps in region-specific reduction in neuronal activation continuously administered via osmotic pumps in region-specific reduction in neuronal activation continuously administered via osmotic pumps in was observed in the hippocampus, caudal and mice from 6 weeks of age until euthanasia. Wild was observed in the hippocampus, caudal and mice from 6 weeks of age until euthanasia. Wild was observed in the hippocampus, caudal and mice from 6 weeks of age until euthanasia. Wild rostral retrosplenial cortices and anterior type mice were subjected to GCV and stroke as rostral retrosplenial cortices and anterior type mice were subjected to GCV and stroke as rostral retrosplenial cortices and anterior type mice were subjected to GCV and stroke as cingulate cortices, medial and lateral entorhinal controls. We found that following 4 weeks of cingulate cortices, medial and lateral entorhinal controls. We found that following 4 weeks of cingulate cortices, medial and lateral entorhinal controls. We found that following 4 weeks of cortices, and in the anteromedial and GCV treatment, both type-1 and type-2 cortices, and in the anteromedial and GCV treatment, both type-1 and type-2 cortices, and in the anteromedial and GCV treatment, both type-1 and type-2 anteroventral thalamic nuclei during spatial progenitor cells were reduced by 70% in the anteroventral thalamic nuclei during spatial progenitor cells were reduced by 70% in the anteroventral thalamic nuclei during spatial progenitor cells were reduced by 70% in the exploration in dMCAO animals compared to dentate gyrus (DG) of sham mice. Although exploration in dMCAO animals compared to dentate gyrus (DG) of sham mice. Although exploration in dMCAO animals compared to dentate gyrus (DG) of sham mice. Although sham animals. Stroke-induced hypoactivation dMCAO induced proliferation of type-1 and sham animals. Stroke-induced hypoactivation dMCAO induced proliferation of type-1 and sham animals. Stroke-induced hypoactivation dMCAO induced proliferation of type-1 and during spatial exploration was not observed in type-2 progenitor cells, there was still a 60% during spatial exploration was not observed in type-2 progenitor cells, there was still a 60% during spatial exploration was not observed in type-2 progenitor cells, there was still a 60% control regions, such as the periaqueductal gray, reduction of DG progenitor cells in the presence control regions, such as the periaqueductal gray, reduction of DG progenitor cells in the presence control regions, such as the periaqueductal gray, reduction of DG progenitor cells in the presence suggesting that they are not a part of the spatial of GCV compared to mice treated with saline. suggesting that they are not a part of the spatial of GCV compared to mice treated with saline. suggesting that they are not a part of the spatial of GCV compared to mice treated with saline. recognition network. Structural connectivity Surprisingly, mice with conditional ablation of recognition network. Structural connectivity Surprisingly, mice with conditional ablation of recognition network. Structural connectivity Surprisingly, mice with conditional ablation of among regions identified in this study and their neuroprogenitor cells did not exhibit an increase among regions identified in this study and their neuroprogenitor cells did not exhibit an increase among regions identified in this study and their neuroprogenitor cells did not exhibit an increase relationship to the parietal cortex warrant further in lesion size. Transgenic mice subjected to relationship to the parietal cortex warrant further in lesion size. Transgenic mice subjected to relationship to the parietal cortex warrant further in lesion size. Transgenic mice subjected to validation. stroke and GCV displayed impaired spatial validation. stroke and GCV displayed impaired spatial validation. stroke and GCV displayed impaired spatial learning and memory in the Barnes maze test learning and memory in the Barnes maze test learning and memory in the Barnes maze test P-34 Reduction of Neuroprogenitor Cells In compared to saline control or wild type mice P-34 Reduction of Neuroprogenitor Cells In compared to saline control or wild type mice P-34 Reduction of Neuroprogenitor Cells In compared to saline control or wild type mice Mice Impedes Post-Stroke Functional subjected to GCV and stroke, suggesting that Mice Impedes Post-Stroke Functional subjected to GCV and stroke, suggesting that Mice Impedes Post-Stroke Functional subjected to GCV and stroke, suggesting that Recovery the observed functional impairment was a Recovery the observed functional impairment was a Recovery the observed functional impairment was a

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 55 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 55 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 55 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE consequence of inhibiting neurogenesis and was spared the hippocampus, while ICH produced consequence of inhibiting neurogenesis and was spared the hippocampus, while ICH produced consequence of inhibiting neurogenesis and was spared the hippocampus, while ICH produced not related to the toxicity of GCV. However, exclusive damage to the internal capsule and not related to the toxicity of GCV. However, exclusive damage to the internal capsule and not related to the toxicity of GCV. However, exclusive damage to the internal capsule and there was no significant difference in post- striatum. sMCAO led to cortical and subcortical there was no significant difference in post- striatum. sMCAO led to cortical and subcortical there was no significant difference in post- striatum. sMCAO led to cortical and subcortical stroke motor function between transgenic mice lesions with only minor cell loss in the CA1. stroke motor function between transgenic mice lesions with only minor cell loss in the CA1. stroke motor function between transgenic mice lesions with only minor cell loss in the CA1. treated with GCV and those treated with Spatial exploration in sham significantly treated with GCV and those treated with Spatial exploration in sham significantly treated with GCV and those treated with Spatial exploration in sham significantly vehicle. Our data suggest a contributing role of increased Fos expression in all subfields of the vehicle. Our data suggest a contributing role of increased Fos expression in all subfields of the vehicle. Our data suggest a contributing role of increased Fos expression in all subfields of the stroke-induced neurogenesis in the recovery of hippocampus. In contrast, hippocampal stroke-induced neurogenesis in the recovery of hippocampus. In contrast, hippocampal stroke-induced neurogenesis in the recovery of hippocampus. In contrast, hippocampal cognitive function. hypoactivation occurred in rats with either cognitive function. hypoactivation occurred in rats with either cognitive function. hypoactivation occurred in rats with either ischemic or hemorrhagic stroke in a region ischemic or hemorrhagic stroke in a region ischemic or hemorrhagic stroke in a region P-35 Experimental ischemic and specific manner. Fos activation was not affected P-35 Experimental ischemic and specific manner. Fos activation was not affected P-35 Experimental ischemic and specific manner. Fos activation was not affected hemorrhagic strokes induce memory in regions that were not involved in processing hemorrhagic strokes induce memory in regions that were not involved in processing hemorrhagic strokes induce memory in regions that were not involved in processing impairment and reduce hippocampal spatial information during spatial exploration, impairment and reduce hippocampal spatial information during spatial exploration, impairment and reduce hippocampal spatial information during spatial exploration, functional recruitment during spatial indicating that the observed effects were region functional recruitment during spatial indicating that the observed effects were region functional recruitment during spatial indicating that the observed effects were region navigation and task-specific rather than a generalized navigation and task-specific rather than a generalized navigation and task-specific rather than a generalized metabolic depression. Further, reduced metabolic depression. Further, reduced metabolic depression. Further, reduced C.C.J. Lee1, 2, Y. Wang1, 2, 3, W. Liu1, 2, 3, C. Sun1, hippocampal recruitment during spatial C.C.J. Lee1, 2, Y. Wang1, 2, 3, W. Liu1, 2, 3, C. Sun1, hippocampal recruitment during spatial C.C.J. Lee1, 2, Y. Wang1, 2, 3, W. Liu1, 2, 3, C. Sun1, hippocampal recruitment during spatial 2, S. Badurek1, 2, S. Wu1, 2, C. Burger1, 2 , J. Liu1, exploration in stroke rats predicted the 2, S. Badurek1, 2, S. Wu1, 2, C. Burger1, 2 , J. Liu1, exploration in stroke rats predicted the 2, S. Badurek1, 2, S. Wu1, 2, C. Burger1, 2 , J. Liu1, exploration in stroke rats predicted the 2 magnitude of memory impairment assessed by 2 magnitude of memory impairment assessed by 2 magnitude of memory impairment assessed by Department of Neurological Surgery1, the Barnes maze test. Department of Neurological Surgery1, the Barnes maze test. Department of Neurological Surgery1, the Barnes maze test. UCSF and SFVAMC2, San Francisco, UCSF and SFVAMC2, San Francisco, UCSF and SFVAMC2, San Francisco, California; Department of Neurological P-36 Unexpected Neuronal Loss After California; Department of Neurological P-36 Unexpected Neuronal Loss After California; Department of Neurological P-36 Unexpected Neuronal Loss After Surgery3, Beijing Tiantan Hospital, Capital Spinal Cord Injections In Primates Surgery3, Beijing Tiantan Hospital, Capital Spinal Cord Injections In Primates Surgery3, Beijing Tiantan Hospital, Capital Spinal Cord Injections In Primates Medical University, Beijing, P R China Medical University, Beijing, P R China Medical University, Beijing, P R China E. S. Rosenzweig1*, G. Courtine2,3, J. H. Brock1, E. S. Rosenzweig1*, G. Courtine2,3, J. H. Brock1, E. S. Rosenzweig1*, G. Courtine2,3, J. H. Brock1, Cognitive impairment is a frequent, but a Y. S. Nout4, A. R. Ferguson4, J. L. Nielson4, S. Cognitive impairment is a frequent, but a Y. S. Nout4, A. R. Ferguson4, J. L. Nielson4, S. Cognitive impairment is a frequent, but a Y. S. Nout4, A. R. Ferguson4, J. L. Nielson4, S. commonly neglected consequence after stroke. C. Strand5, R. Moseanko5, S. Hawbecker5, R. R. commonly neglected consequence after stroke. C. Strand5, R. Moseanko5, S. Hawbecker5, R. R. commonly neglected consequence after stroke. C. Strand5, R. Moseanko5, S. Hawbecker5, R. R. Hippocampal dysfunction occurs following Roy2, H. Zhong2, J. L. Weber1, M. S. Beattie4, L. Hippocampal dysfunction occurs following Roy2, H. Zhong2, J. L. Weber1, M. S. Beattie4, L. Hippocampal dysfunction occurs following Roy2, H. Zhong2, J. L. Weber1, M. S. Beattie4, L. injury to remote brain regions such as the A. Havton6, V. R. Edgerton2, J. C. Bresnahan4, injury to remote brain regions such as the A. Havton6, V. R. Edgerton2, J. C. Bresnahan4, injury to remote brain regions such as the A. Havton6, V. R. Edgerton2, J. C. Bresnahan4, anterior thalamus or fornix. The current study O. Steward7, and M. H. Tuszynski1,8 anterior thalamus or fornix. The current study O. Steward7, and M. H. Tuszynski1,8 anterior thalamus or fornix. The current study O. Steward7, and M. H. Tuszynski1,8 aims to determine whether stroke involving 1Dept. of Neurosciences, University of aims to determine whether stroke involving 1Dept. of Neurosciences, University of aims to determine whether stroke involving 1Dept. of Neurosciences, University of sensorimotor cortex (SMC) or basic ganglia California - San Diego, La Jolla, CA; 2 Depts. sensorimotor cortex (SMC) or basic ganglia California - San Diego, La Jolla, CA; 2 Depts. sensorimotor cortex (SMC) or basic ganglia California - San Diego, La Jolla, CA; 2 Depts. (BG) affects hippocampal activation during of Integrative Biology and Physiology and (BG) affects hippocampal activation during of Integrative Biology and Physiology and (BG) affects hippocampal activation during of Integrative Biology and Physiology and spatial navigation and subsequent learning and Neurobiology, University of California, Los spatial navigation and subsequent learning and Neurobiology, University of California, Los spatial navigation and subsequent learning and Neurobiology, University of California, Los memory function. Ischemic stroke was induced Angeles, CA; 3Dept. of Neurology, University of memory function. Ischemic stroke was induced Angeles, CA; 3Dept. of Neurology, University of memory function. Ischemic stroke was induced Angeles, CA; 3Dept. of Neurology, University of by the occlusion of middle cerebral artery Zurich, Zurich, Switzerland; 4Dept. of by the occlusion of middle cerebral artery Zurich, Zurich, Switzerland; 4Dept. of by the occlusion of middle cerebral artery Zurich, Zurich, Switzerland; 4Dept. of (MCA) using either the distal (dMCAO) or the Neurosurgery, University of California, San (MCA) using either the distal (dMCAO) or the Neurosurgery, University of California, San (MCA) using either the distal (dMCAO) or the Neurosurgery, University of California, San intraluminal suture method (sMCAO). Francisco, CA; 5California National Primate intraluminal suture method (sMCAO). Francisco, CA; 5California National Primate intraluminal suture method (sMCAO). Francisco, CA; 5California National Primate Intracerebral hemorrhage (ICH) was produced Research Center, University of California, Intracerebral hemorrhage (ICH) was produced Research Center, University of California, Intracerebral hemorrhage (ICH) was produced Research Center, University of California, by injection of collagenase into the BG. Davis, CA; 6Dept. of Anesthesiology and by injection of collagenase into the BG. Davis, CA; 6Dept. of Anesthesiology and by injection of collagenase into the BG. Davis, CA; 6Dept. of Anesthesiology and Functional recruitment of hippocampal circuitry Perioperative Care, University of California - Functional recruitment of hippocampal circuitry Perioperative Care, University of California - Functional recruitment of hippocampal circuitry Perioperative Care, University of California - was determined by mapping/quantifying the Fos Irvine, Irvine, CA; 7Dept. of Neurobiology, was determined by mapping/quantifying the Fos Irvine, Irvine, CA; 7Dept. of Neurobiology, was determined by mapping/quantifying the Fos Irvine, Irvine, CA; 7Dept. of Neurobiology, expression during spatial exploration of a University of California - Irvine, Irvine, CA; expression during spatial exploration of a University of California - Irvine, Irvine, CA; expression during spatial exploration of a University of California - Irvine, Irvine, CA; circular arena 5 days after stroke or sham 8Veterans Administration Medical Center, La circular arena 5 days after stroke or sham 8Veterans Administration Medical Center, La circular arena 5 days after stroke or sham 8Veterans Administration Medical Center, La surgery. Spatial memory was assessed at 7-8 Jolla, CA surgery. Spatial memory was assessed at 7-8 Jolla, CA surgery. Spatial memory was assessed at 7-8 Jolla, CA weeks after stroke or sham by the Barnes maze weeks after stroke or sham by the Barnes maze weeks after stroke or sham by the Barnes maze test. dMCAO primarily affected the SMC and test. dMCAO primarily affected the SMC and test. dMCAO primarily affected the SMC and

56 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 56 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 56 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

Safe delivery of therapeutic substances Supported by NIH R01-NS042291, VA Safe delivery of therapeutic substances Supported by NIH R01-NS042291, VA Safe delivery of therapeutic substances Supported by NIH R01-NS042291, VA to the nervous system is critical when B7332R, Roman Reed Foundation 10-274, the to the nervous system is critical when B7332R, Roman Reed Foundation 10-274, the to the nervous system is critical when B7332R, Roman Reed Foundation 10-274, the translating candidate treatments to humans, but Dr. Miriam & Sheldon G. Adelson Medical translating candidate treatments to humans, but Dr. Miriam & Sheldon G. Adelson Medical translating candidate treatments to humans, but Dr. Miriam & Sheldon G. Adelson Medical the difficulty and expense of primate models Research Foundation, and the Bernard and Anne the difficulty and expense of primate models Research Foundation, and the Bernard and Anne the difficulty and expense of primate models Research Foundation, and the Bernard and Anne often limits translational testing to smaller Spitzer Charitable Trust. often limits translational testing to smaller Spitzer Charitable Trust. often limits translational testing to smaller Spitzer Charitable Trust. species. As part of a program to study therapies species. As part of a program to study therapies species. As part of a program to study therapies for spinal cord injury, we injected candidate P-37 Long-Distance Axonal Growth, for spinal cord injury, we injected candidate P-37 Long-Distance Axonal Growth, for spinal cord injury, we injected candidate P-37 Long-Distance Axonal Growth, therapeutics into the spinal cord of Rhesus Connectivity and Functional Recovery After therapeutics into the spinal cord of Rhesus Connectivity and Functional Recovery After therapeutics into the spinal cord of Rhesus Connectivity and Functional Recovery After macaques following C7 spinal cord hemisection Complete Spinal Cord Transection: Cell- macaques following C7 spinal cord hemisection Complete Spinal Cord Transection: Cell- macaques following C7 spinal cord hemisection Complete Spinal Cord Transection: Cell- lesions. Test substances included various Intrinsic Mechanisms Overcome Inhibition lesions. Test substances included various Intrinsic Mechanisms Overcome Inhibition lesions. Test substances included various Intrinsic Mechanisms Overcome Inhibition mixtures of adeno-associated viral vectors Of The Adult Lesioned Spinal Cord mixtures of adeno-associated viral vectors Of The Adult Lesioned Spinal Cord mixtures of adeno-associated viral vectors Of The Adult Lesioned Spinal Cord (encoding green fluorescent protein, brain- (encoding green fluorescent protein, brain- (encoding green fluorescent protein, brain- derived neurotrophic factor, or neurotrophin-3) J.H. Brock1, P. Lu1,2, Y. Wang1, L. Graham1, K. derived neurotrophic factor, or neurotrophin-3) J.H. Brock1, P. Lu1,2, Y. Wang1, L. Graham1, K. derived neurotrophic factor, or neurotrophin-3) J.H. Brock1, P. Lu1,2, Y. Wang1, L. Graham1, K. and chondroitinase. We injected 5 µl of test McHale1, M. , Gao1, D. Wu1, , L.A. Havton3, A. and chondroitinase. We injected 5 µl of test McHale1, M. , Gao1, D. Wu1, , L.A. Havton3, A. and chondroitinase. We injected 5 µl of test McHale1, M. , Gao1, D. Wu1, , L.A. Havton3, A. substance through glass micropipettes into Blesch1, 4, B. Zheng1, J.M. Conner1, and M.H. substance through glass micropipettes into Blesch1, 4, B. Zheng1, J.M. Conner1, and M.H. substance through glass micropipettes into Blesch1, 4, B. Zheng1, J.M. Conner1, and M.H. spinal cord gray matter below the hemisection at Tuszynski1,2 spinal cord gray matter below the hemisection at Tuszynski1,2 spinal cord gray matter below the hemisection at Tuszynski1,2 each of 10 sites per monkey. Infusions were 1Dept. of Neurosciences, University of each of 10 sites per monkey. Infusions were 1Dept. of Neurosciences, University of each of 10 sites per monkey. Infusions were 1Dept. of Neurosciences, University of made at low rates (0.5 µl/min) using a Nano- California - San Diego, La Jolla, CA; made at low rates (0.5 µl/min) using a Nano- California - San Diego, La Jolla, CA; made at low rates (0.5 µl/min) using a Nano- California - San Diego, La Jolla, CA; injector syringe pump (N=9 monkeys) or a 2 Veterans Administration Medical Center, La injector syringe pump (N=9 monkeys) or a 2 Veterans Administration Medical Center, La injector syringe pump (N=9 monkeys) or a 2 Veterans Administration Medical Center, La Picospritzer at pressures under 20 dynes (N=7). Jolla, CA; 3 Dept. of Neurology, University of Picospritzer at pressures under 20 dynes (N=7). Jolla, CA; 3 Dept. of Neurology, University of Picospritzer at pressures under 20 dynes (N=7). Jolla, CA; 3 Dept. of Neurology, University of Eight ‘Uninjected’ controls received lesions and California, Los Angeles, CA; 4 Spinal Cord Eight ‘Uninjected’ controls received lesions and California, Los Angeles, CA; 4 Spinal Cord Eight ‘Uninjected’ controls received lesions and California, Los Angeles, CA; 4 Spinal Cord either no injections (N=6), needle entry only Injury Center, Heidelberg University Hospital, either no injections (N=6), needle entry only Injury Center, Heidelberg University Hospital, either no injections (N=6), needle entry only Injury Center, Heidelberg University Hospital, (N=1) or saline injection (N=1; designated Germany (N=1) or saline injection (N=1; designated Germany (N=1) or saline injection (N=1; designated Germany ‘Control’ a priori). Subjects performed a battery ‘Control’ a priori). Subjects performed a battery ‘Control’ a priori). Subjects performed a battery of functional tests and were sacrificed 6 months We grafted embryonic spinal cord neural of functional tests and were sacrificed 6 months We grafted embryonic spinal cord neural of functional tests and were sacrificed 6 months We grafted embryonic spinal cord neural after SCI. Qualitative evaluation of spinal cord cells from green fluorescent protein (GFP)- after SCI. Qualitative evaluation of spinal cord cells from green fluorescent protein (GFP)- after SCI. Qualitative evaluation of spinal cord cells from green fluorescent protein (GFP)- tissue labeled for Nissl substance, choline expressing rats into sites of adult spinal cord tissue labeled for Nissl substance, choline expressing rats into sites of adult spinal cord tissue labeled for Nissl substance, choline expressing rats into sites of adult spinal cord acetyltransferase, or neuron-specific nuclear injury. Grafted embryonic neurons extended acetyltransferase, or neuron-specific nuclear injury. Grafted embryonic neurons extended acetyltransferase, or neuron-specific nuclear injury. Grafted embryonic neurons extended protein (NeuN) showed a dramatic loss of spinal large numbers of axons into the adult spinal protein (NeuN) showed a dramatic loss of spinal large numbers of axons into the adult spinal protein (NeuN) showed a dramatic loss of spinal large numbers of axons into the adult spinal cord neurons in all subjects receiving injections cord over remarkably long distances. Axons cord neurons in all subjects receiving injections cord over remarkably long distances. Axons cord neurons in all subjects receiving injections cord over remarkably long distances. Axons of any substance (except saline) into the spinal extended rostrally from a mid-cervical lesion of any substance (except saline) into the spinal extended rostrally from a mid-cervical lesion of any substance (except saline) into the spinal extended rostrally from a mid-cervical lesion cord. Stereological analysis of NeuN-labeled site into the brainstem, and caudally over more cord. Stereological analysis of NeuN-labeled site into the brainstem, and caudally over more cord. Stereological analysis of NeuN-labeled site into the brainstem, and caudally over more nuclei revealed 58±6% loss (compared to the than half the distance of the remaining spinal nuclei revealed 58±6% loss (compared to the than half the distance of the remaining spinal nuclei revealed 58±6% loss (compared to the than half the distance of the remaining spinal contralateral, intact side of the spinal cord), cord; axons of grafted neurons also exited the contralateral, intact side of the spinal cord), cord; axons of grafted neurons also exited the contralateral, intact side of the spinal cord), cord; axons of grafted neurons also exited the while the Uninjected group showed no neuronal spinal cord and regenerated into ventral motor while the Uninjected group showed no neuronal spinal cord and regenerated into ventral motor while the Uninjected group showed no neuronal spinal cord and regenerated into ventral motor loss. Injected animals had more severe motor roots. Grafted neurons differentiated into loss. Injected animals had more severe motor roots. Grafted neurons differentiated into loss. Injected animals had more severe motor roots. Grafted neurons differentiated into deficits than Uninjected controls, and Principal multiple neuronal phenotypes, including motor deficits than Uninjected controls, and Principal multiple neuronal phenotypes, including motor deficits than Uninjected controls, and Principal multiple neuronal phenotypes, including motor Components Analysis revealed a strong neurons. Axons emerging from grafts formed Components Analysis revealed a strong neurons. Axons emerging from grafts formed Components Analysis revealed a strong neurons. Axons emerging from grafts formed relationship between the degree of neuronal loss abundant synapses of both excitatory and relationship between the degree of neuronal loss abundant synapses of both excitatory and relationship between the degree of neuronal loss abundant synapses of both excitatory and and impairment of forelimb function. Studies inhibitory phenotypes with host neurons. The and impairment of forelimb function. Studies inhibitory phenotypes with host neurons. The and impairment of forelimb function. Studies inhibitory phenotypes with host neurons. The are underway to determine the mechanisms density but not distance of axon outgrowth was are underway to determine the mechanisms density but not distance of axon outgrowth was are underway to determine the mechanisms density but not distance of axon outgrowth was underlying the neuronal loss. These results, not enhanced by viral delivery of brain-derived underlying the neuronal loss. These results, not enhanced by viral delivery of brain-derived underlying the neuronal loss. These results, not enhanced by viral delivery of brain-derived predicted by rodent models, raise important neurotrophic factor (BDNF). Axonal growth predicted by rodent models, raise important neurotrophic factor (BDNF). Axonal growth predicted by rodent models, raise important neurotrophic factor (BDNF). Axonal growth concerns about safety in several ongoing human was partly dependent on the mammalian target concerns about safety in several ongoing human was partly dependent on the mammalian target concerns about safety in several ongoing human was partly dependent on the mammalian target clinical trials, and highlight the need to test of rapamycin (mTOR) signaling. Grafted cells clinical trials, and highlight the need to test of rapamycin (mTOR) signaling. Grafted cells clinical trials, and highlight the need to test of rapamycin (mTOR) signaling. Grafted cells delivery methods in non-human primates. supported formation of functional delivery methods in non-human primates. supported formation of functional delivery methods in non-human primates. supported formation of functional

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 57 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 57 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 57 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE electrophysiological relays across sites of min post-AIH; n=8; p<0.05). Tidal volume (via electrophysiological relays across sites of min post-AIH; n=8; p<0.05). Tidal volume (via electrophysiological relays across sites of min post-AIH; n=8; p<0.05). Tidal volume (via complete thoracic spinal cord transection, plethysmography) is reduced following a C2HS complete thoracic spinal cord transection, plethysmography) is reduced following a C2HS complete thoracic spinal cord transection, plethysmography) is reduced following a C2HS resulting in significant functional recovery. (vs pre-injury values) during normocapnia (- resulting in significant functional recovery. (vs pre-injury values) during normocapnia (- resulting in significant functional recovery. (vs pre-injury values) during normocapnia (- Spinal re-transection immediately above the 29% baseline; p<0.05), hypercapnia (-32% Spinal re-transection immediately above the 29% baseline; p<0.05), hypercapnia (-32% Spinal re-transection immediately above the 29% baseline; p<0.05), hypercapnia (-32% graft implantation site abolished all recovery. baseline, p<0.05) and hypercapnia/hypoxia (- graft implantation site abolished all recovery. baseline, p<0.05) and hypercapnia/hypoxia (- graft implantation site abolished all recovery. baseline, p<0.05) and hypercapnia/hypoxia (- These findings indicate that intrinsic neuronal 30% baseline, p<0.05). dAIH significantly These findings indicate that intrinsic neuronal 30% baseline, p<0.05). dAIH significantly These findings indicate that intrinsic neuronal 30% baseline, p<0.05). dAIH significantly properties can overcome the inhibitory milieu of improves tidal volume capacity (normocapnia: properties can overcome the inhibitory milieu of improves tidal volume capacity (normocapnia: properties can overcome the inhibitory milieu of improves tidal volume capacity (normocapnia: the injured adult CNS to mount remarkably 83%, hypercapnia: 82% and the injured adult CNS to mount remarkably 83%, hypercapnia: 82% and the injured adult CNS to mount remarkably 83%, hypercapnia: 82% and robust axonal growth resulting in formation of hypercapnia/hypoxia: 85% of pre-injury values; robust axonal growth resulting in formation of hypercapnia/hypoxia: 85% of pre-injury values; robust axonal growth resulting in formation of hypercapnia/hypoxia: 85% of pre-injury values; novel relay circuits that restore function. p<0.05). This significant improvement is novel relay circuits that restore function. p<0.05). This significant improvement is novel relay circuits that restore function. p<0.05). This significant improvement is Supported by the Veterans Administration, NIH observed up to 2 weeks following the end of Supported by the Veterans Administration, NIH observed up to 2 weeks following the end of Supported by the Veterans Administration, NIH observed up to 2 weeks following the end of (NS09881), Wings for Life, Canadian Spinal dAIH. dAIH increases serotonergic terminal (NS09881), Wings for Life, Canadian Spinal dAIH. dAIH increases serotonergic terminal (NS09881), Wings for Life, Canadian Spinal dAIH. dAIH increases serotonergic terminal Research Organization, the Craig Neilsen size and 5HT2A receptor density near phrenic Research Organization, the Craig Neilsen size and 5HT2A receptor density near phrenic Research Organization, the Craig Neilsen size and 5HT2A receptor density near phrenic Foundation, the Swiss Institute for Research motoneurons contralateral to injury (p<0.05). Foundation, the Swiss Institute for Research motoneurons contralateral to injury (p<0.05). Foundation, the Swiss Institute for Research motoneurons contralateral to injury (p<0.05). into Paraplegia, and the Dr. Miriam and Sheldon However, pre-treatment with the broad spectrum into Paraplegia, and the Dr. Miriam and Sheldon However, pre-treatment with the broad spectrum into Paraplegia, and the Dr. Miriam and Sheldon However, pre-treatment with the broad spectrum G. Adelson Medical Research Foundation. serotonin receptor antagonist methysergide prior G. Adelson Medical Research Foundation. serotonin receptor antagonist methysergide prior G. Adelson Medical Research Foundation. serotonin receptor antagonist methysergide prior to AIH on each day of the dAIH protocol had no to AIH on each day of the dAIH protocol had no to AIH on each day of the dAIH protocol had no P-38 Daily Acute Intermittent Hypoxia effect on tidal volume recovery, suggesting that P-38 Daily Acute Intermittent Hypoxia effect on tidal volume recovery, suggesting that P-38 Daily Acute Intermittent Hypoxia effect on tidal volume recovery, suggesting that Restores Respiratory Plasticity And the effects of dAIH do not require serotonin Restores Respiratory Plasticity And the effects of dAIH do not require serotonin Restores Respiratory Plasticity And the effects of dAIH do not require serotonin Breathing Capacity Following Cervical receptor activation. Thus, dAIH may be a useful Breathing Capacity Following Cervical receptor activation. Thus, dAIH may be a useful Breathing Capacity Following Cervical receptor activation. Thus, dAIH may be a useful Injury therapeutic approach to increase breathing Injury therapeutic approach to increase breathing Injury therapeutic approach to increase breathing capacity, although its mechanism of action capacity, although its mechanism of action capacity, although its mechanism of action S. Vinit, J. Terada, P.M. MacFarlane, G.S. remains unknown. dAIH may have potential as S. Vinit, J. Terada, P.M. MacFarlane, G.S. remains unknown. dAIH may have potential as S. Vinit, J. Terada, P.M. MacFarlane, G.S. remains unknown. dAIH may have potential as Mitchell a treatment for spinal injury or Mitchell a treatment for spinal injury or Mitchell a treatment for spinal injury or University of Wisconsin-Madison, USA. neurodegenerative diseases that lead to University of Wisconsin-Madison, USA. neurodegenerative diseases that lead to University of Wisconsin-Madison, USA. neurodegenerative diseases that lead to respiratory insufficiency. Supported by NIH respiratory insufficiency. Supported by NIH respiratory insufficiency. Supported by NIH Acute intermittent hypoxia (AIH) elicits HL69064, Craig H Neilsen Foundation. Acute intermittent hypoxia (AIH) elicits HL69064, Craig H Neilsen Foundation. Acute intermittent hypoxia (AIH) elicits HL69064, Craig H Neilsen Foundation. a form of serotonin-dependent respiratory a form of serotonin-dependent respiratory a form of serotonin-dependent respiratory plasticity in phrenic nerve activity in P-39 Molecular Mechanisms involved in plasticity in phrenic nerve activity in P-39 Molecular Mechanisms involved in plasticity in phrenic nerve activity in P-39 Molecular Mechanisms involved in anesthetized rats known as phrenic long-term Recovery of Respiration after Upper cervical anesthetized rats known as phrenic long-term Recovery of Respiration after Upper cervical anesthetized rats known as phrenic long-term Recovery of Respiration after Upper cervical facilitation (pLTF). After chronic C2 Spinal Cord Injury: Potential Therapeutic facilitation (pLTF). After chronic C2 Spinal Cord Injury: Potential Therapeutic facilitation (pLTF). After chronic C2 Spinal Cord Injury: Potential Therapeutic hemisection (C2HS), AIH elicits pLTF Strategies. hemisection (C2HS), AIH elicits pLTF Strategies. hemisection (C2HS), AIH elicits pLTF Strategies. ipsilateral (Golder and Mitchell, 2005), but not ipsilateral (Golder and Mitchell, 2005), but not ipsilateral (Golder and Mitchell, 2005), but not contralateral to injury (Doperalski and Fuller, K. D. Nantwi, and L. P. Singh contralateral to injury (Doperalski and Fuller, K. D. Nantwi, and L. P. Singh contralateral to injury (Doperalski and Fuller, K. D. Nantwi, and L. P. Singh 2006). Since respiratory LTF is enhanced by Department of Anatomy and Cell 2006). Since respiratory LTF is enhanced by Department of Anatomy and Cell 2006). Since respiratory LTF is enhanced by Department of Anatomy and Cell repetitive exposure to AIH, we hypothesized Biology, Wayne State University, School of repetitive exposure to AIH, we hypothesized Biology, Wayne State University, School of repetitive exposure to AIH, we hypothesized Biology, Wayne State University, School of that daily AIH (dAIH, 7 days; 10-5 min Medicine, Detroit, MI 48202 that daily AIH (dAIH, 7 days; 10-5 min Medicine, Detroit, MI 48202 that daily AIH (dAIH, 7 days; 10-5 min Medicine, Detroit, MI 48202 episodes of 11% O2, 5 min normoxic intervals) episodes of 11% O2, 5 min normoxic intervals) episodes of 11% O2, 5 min normoxic intervals) would restore the pLTF contralateral to C2HS Previous studies have demonstrated that would restore the pLTF contralateral to C2HS Previous studies have demonstrated that would restore the pLTF contralateral to C2HS Previous studies have demonstrated that and increase the tidal volume capacity in functional recovery of respiratory activity in an and increase the tidal volume capacity in functional recovery of respiratory activity in an and increase the tidal volume capacity in functional recovery of respiratory activity in an unanesthetized rats. Following AIH, no pLTF animal model (HC2) of SCI can be unanesthetized rats. Following AIH, no pLTF animal model (HC2) of SCI can be unanesthetized rats. Following AIH, no pLTF animal model (HC2) of SCI can be was observed in untreated rats contralateral to pharmacologically induced. In this model, was observed in untreated rats contralateral to pharmacologically induced. In this model, was observed in untreated rats contralateral to pharmacologically induced. In this model, C2HS (7% ± 4% of hypoxic activity, 60 min activity in the hemidiaphragm rendered C2HS (7% ± 4% of hypoxic activity, 60 min activity in the hemidiaphragm rendered C2HS (7% ± 4% of hypoxic activity, 60 min activity in the hemidiaphragm rendered post-AIH; n=6; n.s.). In contrast, robust pLTF quiescent by injury can be restored by systemic post-AIH; n=6; n.s.). In contrast, robust pLTF quiescent by injury can be restored by systemic post-AIH; n=6; n.s.). In contrast, robust pLTF quiescent by injury can be restored by systemic was observed contralateral to injury in dAIH administration of theophylline via (1) activation was observed contralateral to injury in dAIH administration of theophylline via (1) activation was observed contralateral to injury in dAIH administration of theophylline via (1) activation treated rats (33% ± 11% of hypoxic activity, 60 of cyclic AMP-induced CREB-phosphorylation treated rats (33% ± 11% of hypoxic activity, 60 of cyclic AMP-induced CREB-phosphorylation treated rats (33% ± 11% of hypoxic activity, 60 of cyclic AMP-induced CREB-phosphorylation

58 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 58 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 58 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE or lithium chloride via (2) activation of the D.E. Sanchez, K. Salazar, L.M. Mercier, B.E. or lithium chloride via (2) activation of the D.E. Sanchez, K. Salazar, L.M. Mercier, B.E. or lithium chloride via (2) activation of the D.E. Sanchez, K. Salazar, L.M. Mercier, B.E. GSKβ phosphorylation pathway. Our studies O’Steen, P.J. Reier, M.A. Lane GSKβ phosphorylation pathway. Our studies O’Steen, P.J. Reier, M.A. Lane GSKβ phosphorylation pathway. Our studies O’Steen, P.J. Reier, M.A. Lane have identified molecular signals and Department of Neuroscience, McKnight have identified molecular signals and Department of Neuroscience, McKnight have identified molecular signals and Department of Neuroscience, McKnight neurotrophic factors (BDNF, GDNF, and Bcl2) Brain Institute, University of Florida, PO Box neurotrophic factors (BDNF, GDNF, and Bcl2) Brain Institute, University of Florida, PO Box neurotrophic factors (BDNF, GDNF, and Bcl2) Brain Institute, University of Florida, PO Box in both pathways that may mediate recovery. 100244, Gainesville, Florida, 32611 in both pathways that may mediate recovery. 100244, Gainesville, Florida, 32611 in both pathways that may mediate recovery. 100244, Gainesville, Florida, 32611 Although it is also known that inflammatory Although it is also known that inflammatory Although it is also known that inflammatory signals are triggered following injury, it remains Mid-cervical spinal cord injuries (SCI) signals are triggered following injury, it remains Mid-cervical spinal cord injuries (SCI) signals are triggered following injury, it remains Mid-cervical spinal cord injuries (SCI) unclear whether inflammatory events/signals, can impair breathing due to disruption of unclear whether inflammatory events/signals, can impair breathing due to disruption of unclear whether inflammatory events/signals, can impair breathing due to disruption of may mitigate against recovery. The objectives bulbospinal respiratory fiber pathways and loss may mitigate against recovery. The objectives bulbospinal respiratory fiber pathways and loss may mitigate against recovery. The objectives bulbospinal respiratory fiber pathways and loss of the present study are: (1) to identify of phrenic motoneurons (PhMNs) and pre- of the present study are: (1) to identify of phrenic motoneurons (PhMNs) and pre- of the present study are: (1) to identify of phrenic motoneurons (PhMNs) and pre- inflammatory signals triggered after injury and phrenic interneurons. Diminished diaphragm inflammatory signals triggered after injury and phrenic interneurons. Diminished diaphragm inflammatory signals triggered after injury and phrenic interneurons. Diminished diaphragm (2) to assess whether early resolution of EMG (diaEMG) response is a consistent (2) to assess whether early resolution of EMG (diaEMG) response is a consistent (2) to assess whether early resolution of EMG (diaEMG) response is a consistent inflammatory processes by neurotrophic factors outcome following respiratory challenge (e.g. inflammatory processes by neurotrophic factors outcome following respiratory challenge (e.g. inflammatory processes by neurotrophic factors outcome following respiratory challenge (e.g. underlies recovery. Briefly, adult female hypercapnia) and recent evidence suggests that underlies recovery. Briefly, adult female hypercapnia) and recent evidence suggests that underlies recovery. Briefly, adult female hypercapnia) and recent evidence suggests that Sprague-Dawley rats were subjected to a left C2 gray matter injury is the basis for this deficit. Sprague-Dawley rats were subjected to a left C2 gray matter injury is the basis for this deficit. Sprague-Dawley rats were subjected to a left C2 gray matter injury is the basis for this deficit. hemisection (HC2). HC2 rats were divided into This study determines whether restitution of hemisection (HC2). HC2 rats were divided into This study determines whether restitution of hemisection (HC2). HC2 rats were divided into This study determines whether restitution of three groups. Group 1 rats (n=6) were gray matter integrity following injury at the three groups. Group 1 rats (n=6) were gray matter integrity following injury at the three groups. Group 1 rats (n=6) were gray matter integrity following injury at the administered theophylline (20 mg/kg 3X daily level of the PhMN pool would result in administered theophylline (20 mg/kg 3X daily level of the PhMN pool would result in administered theophylline (20 mg/kg 3X daily level of the PhMN pool would result in for 3 days), Group 2 (n=6) received lithium improved diaphragm function. Lateralized C3/4 for 3 days), Group 2 (n=6) received lithium improved diaphragm function. Lateralized C3/4 for 3 days), Group 2 (n=6) received lithium improved diaphragm function. Lateralized C3/4 chloride (85mg/kg daily for 3 days) and Group 3 contusions were produced in adult female rats chloride (85mg/kg daily for 3 days) and Group 3 contusions were produced in adult female rats chloride (85mg/kg daily for 3 days) and Group 3 contusions were produced in adult female rats (n=5) rats were sham-operated controls. All rats using the Infinite Horizon Impactor (200 (n=5) rats were sham-operated controls. All rats using the Infinite Horizon Impactor (200 (n=5) rats were sham-operated controls. All rats using the Infinite Horizon Impactor (200 were prepared for assessment of molecular kilodyne preset force). One week later were prepared for assessment of molecular kilodyne preset force). One week later were prepared for assessment of molecular kilodyne preset force). One week later signals immediately after conclusion of drug dissociated E13.5-14 fetal spinal cord (FSC) signals immediately after conclusion of drug dissociated E13.5-14 fetal spinal cord (FSC) signals immediately after conclusion of drug dissociated E13.5-14 fetal spinal cord (FSC) administration. Spinal cord segments C3-C6 tissue was injected into the lesion epicenter. administration. Spinal cord segments C3-C6 tissue was injected into the lesion epicenter. administration. Spinal cord segments C3-C6 tissue was injected into the lesion epicenter. were excised and sagitally divided into Treated animals were compared with untreated were excised and sagitally divided into Treated animals were compared with untreated were excised and sagitally divided into Treated animals were compared with untreated ipsilateral and contralateral sections and stored controls. Upon recovering one month post- ipsilateral and contralateral sections and stored controls. Upon recovering one month post- ipsilateral and contralateral sections and stored controls. Upon recovering one month post- @ -800 C prior to analysis. In experiments thus transplant, pseudorabies virus was applied @ -800 C prior to analysis. In experiments thus transplant, pseudorabies virus was applied @ -800 C prior to analysis. In experiments thus transplant, pseudorabies virus was applied far, expression of BDNF, GDNF and Bcl2 directly to the diaphragm or injected into the site far, expression of BDNF, GDNF and Bcl2 directly to the diaphragm or injected into the site far, expression of BDNF, GDNF and Bcl2 directly to the diaphragm or injected into the site correlate positively with recovery. Furthermore, of transplantation, to establish connectivity correlate positively with recovery. Furthermore, of transplantation, to establish connectivity correlate positively with recovery. Furthermore, of transplantation, to establish connectivity expression of inflammatory genes such as between 1) donor neurons and the host phrenic expression of inflammatory genes such as between 1) donor neurons and the host phrenic expression of inflammatory genes such as between 1) donor neurons and the host phrenic TXNIP and IL-1β are decreased after drug circuit and 2) host and donor neurons. Animals TXNIP and IL-1β are decreased after drug circuit and 2) host and donor neurons. Animals TXNIP and IL-1β are decreased after drug circuit and 2) host and donor neurons. Animals treatment. This may suggest an early resolution were then left to recover for 24-72 hours treatment. This may suggest an early resolution were then left to recover for 24-72 hours treatment. This may suggest an early resolution were then left to recover for 24-72 hours of inflammation to unravel recovery processes. following PRV delivery. Terminal EMG of inflammation to unravel recovery processes. following PRV delivery. Terminal EMG of inflammation to unravel recovery processes. following PRV delivery. Terminal EMG However, pro-inflammatory cytokine TNF- α recordings were made in spontaneously However, pro-inflammatory cytokine TNF- α recordings were made in spontaneously However, pro-inflammatory cytokine TNF- α recordings were made in spontaneously levels remain up-regulated after injury and breathing animals to assess ipsi- and levels remain up-regulated after injury and breathing animals to assess ipsi- and levels remain up-regulated after injury and breathing animals to assess ipsi- and subsequent drug treatment. We propose that in contralateral diaphragm activity under baseline subsequent drug treatment. We propose that in contralateral diaphragm activity under baseline subsequent drug treatment. We propose that in contralateral diaphragm activity under baseline SCI therapy, it may be beneficial to target (eupneic breathing) and challenge (exposed to SCI therapy, it may be beneficial to target (eupneic breathing) and challenge (exposed to SCI therapy, it may be beneficial to target (eupneic breathing) and challenge (exposed to inhibitory genes that may be persistently hypercapnia) conditions. All injured-untreated inhibitory genes that may be persistently hypercapnia) conditions. All injured-untreated inhibitory genes that may be persistently hypercapnia) conditions. All injured-untreated expressed in response to injury. This strategy animals exhibited blunted ipsilateral EMG expressed in response to injury. This strategy animals exhibited blunted ipsilateral EMG expressed in response to injury. This strategy animals exhibited blunted ipsilateral EMG may further improve recovery processes in SCI. responses to respiratory challenge 5wks post- may further improve recovery processes in SCI. responses to respiratory challenge 5wks post- may further improve recovery processes in SCI. responses to respiratory challenge 5wks post- injury. In contrast, graft recipients showed injury. In contrast, graft recipients showed injury. In contrast, graft recipients showed P-40 Intraspinal grafts of neural elevated EMG activity during challenge. PRV P-40 Intraspinal grafts of neural elevated EMG activity during challenge. PRV P-40 Intraspinal grafts of neural elevated EMG activity during challenge. PRV progenitors improves respiratory function delivered to the ipsilateral hemidiaphragm progenitors improves respiratory function delivered to the ipsilateral hemidiaphragm progenitors improves respiratory function delivered to the ipsilateral hemidiaphragm following mid-cervical contusion injury in resulted in infection of the PhMN pool and following mid-cervical contusion injury in resulted in infection of the PhMN pool and following mid-cervical contusion injury in resulted in infection of the PhMN pool and adult rats second-order host interneurons, as well as adult rats second-order host interneurons, as well as adult rats second-order host interneurons, as well as labeling of a contingent of donor neurons. Intra- labeling of a contingent of donor neurons. Intra- labeling of a contingent of donor neurons. Intra-

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 59 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 59 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 59 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE graft injection of PRV resulted in labeling of exposure to hypoxia). The rats were euthanized graft injection of PRV resulted in labeling of exposure to hypoxia). The rats were euthanized graft injection of PRV resulted in labeling of exposure to hypoxia). The rats were euthanized host interneurons in the vicinity of the grafts. immediately thereafter and host interneurons in the vicinity of the grafts. immediately thereafter and host interneurons in the vicinity of the grafts. immediately thereafter and These data demonstrate that restoration of gray immunocytochemistry was used to examine c- These data demonstrate that restoration of gray immunocytochemistry was used to examine c- These data demonstrate that restoration of gray immunocytochemistry was used to examine c- matter integrity by spinal interneuronal fos expression in brainstem and spinal cord matter integrity by spinal interneuronal fos expression in brainstem and spinal cord matter integrity by spinal interneuronal fos expression in brainstem and spinal cord progenitors can ameliorate an aspect of post- tissue. Transynaptic tracing with pseudorabies progenitors can ameliorate an aspect of post- tissue. Transynaptic tracing with pseudorabies progenitors can ameliorate an aspect of post- tissue. Transynaptic tracing with pseudorabies cervical SCI respiration. Neuroanatomical virus applied to the ipsilateral hemidiaphragm cervical SCI respiration. Neuroanatomical virus applied to the ipsilateral hemidiaphragm cervical SCI respiration. Neuroanatomical virus applied to the ipsilateral hemidiaphragm findings suggest this functional change is was used in a subset of animals to label phrenic findings suggest this functional change is was used in a subset of animals to label phrenic findings suggest this functional change is was used in a subset of animals to label phrenic mediated by bi-directional connectivity between motoneurons and pre-phrenic interneurons ipsi- mediated by bi-directional connectivity between motoneurons and pre-phrenic interneurons ipsi- mediated by bi-directional connectivity between motoneurons and pre-phrenic interneurons ipsi- donor neurons and host interneurons and or contralateral to injury. Very limited c-fos donor neurons and host interneurons and or contralateral to injury. Very limited c-fos donor neurons and host interneurons and or contralateral to injury. Very limited c-fos PhMNs. expression was seen in the cervical cords of PhMNs. expression was seen in the cervical cords of PhMNs. expression was seen in the cervical cords of Supported by: NIH RO1 NS054025 (PJR) and naïve animals. Following exposure to hypoxia, Supported by: NIH RO1 NS054025 (PJR) and naïve animals. Following exposure to hypoxia, Supported by: NIH RO1 NS054025 (PJR) and naïve animals. Following exposure to hypoxia, the Anne and Oscar Lackner Chair in Medicine. however, there was an increase in motoneuron the Anne and Oscar Lackner Chair in Medicine. however, there was an increase in motoneuron the Anne and Oscar Lackner Chair in Medicine. however, there was an increase in motoneuron c-fos staining in the region of the phrenic c-fos staining in the region of the phrenic c-fos staining in the region of the phrenic P-41 Changes In Interneuronal Activity In nucleus, as well as interneuronal labeling in P-41 Changes In Interneuronal Activity In nucleus, as well as interneuronal labeling in P-41 Changes In Interneuronal Activity In nucleus, as well as interneuronal labeling in The Cervical Spinal Cord Of Adult Rats laminae VII and X. This pattern was consistent The Cervical Spinal Cord Of Adult Rats laminae VII and X. This pattern was consistent The Cervical Spinal Cord Of Adult Rats laminae VII and X. This pattern was consistent Following Spinal Cord Injury (SCI) with PRV first- and second-order labeling. A Following Spinal Cord Injury (SCI) with PRV first- and second-order labeling. A Following Spinal Cord Injury (SCI) with PRV first- and second-order labeling. A similar increase in c-fos positive motoneurons similar increase in c-fos positive motoneurons similar increase in c-fos positive motoneurons V.M. Spruance, A.M. Rombola, B.E. O’Steen, and interneurons was observed after respiratory V.M. Spruance, A.M. Rombola, B.E. O’Steen, and interneurons was observed after respiratory V.M. Spruance, A.M. Rombola, B.E. O’Steen, and interneurons was observed after respiratory M.A. Lane, P.J. Reier challenge at two weeks post-C2Hx. These M.A. Lane, P.J. Reier challenge at two weeks post-C2Hx. These M.A. Lane, P.J. Reier challenge at two weeks post-C2Hx. These Department of Neuroscience, College results are consistent with initial Department of Neuroscience, College results are consistent with initial Department of Neuroscience, College results are consistent with initial of Medicine and McKnight Brain Institute, electrophysiological recordings showing of Medicine and McKnight Brain Institute, electrophysiological recordings showing of Medicine and McKnight Brain Institute, electrophysiological recordings showing University of Florida, Gainesville, FL. 32610 cervical interneurons that are responsive to University of Florida, Gainesville, FL. 32610 cervical interneurons that are responsive to University of Florida, Gainesville, FL. 32610 cervical interneurons that are responsive to hypoxia and may thus be responsive to hypoxia and may thus be responsive to hypoxia and may thus be responsive to Cervical SCI can significantly conditions requiring increased respiratory drive Cervical SCI can significantly conditions requiring increased respiratory drive Cervical SCI can significantly conditions requiring increased respiratory drive compromise breathing with the greatest deficits and phrenic motoneuron output. compromise breathing with the greatest deficits and phrenic motoneuron output. compromise breathing with the greatest deficits and phrenic motoneuron output. arising from direct damage to the phrenic circuit Supported by: NIH RO1 NS054025 (PJR), the arising from direct damage to the phrenic circuit Supported by: NIH RO1 NS054025 (PJR), the arising from direct damage to the phrenic circuit Supported by: NIH RO1 NS054025 (PJR), the - controlling diaphragm function. It is known Anne and Oscar Lackner Chair in Medicine - controlling diaphragm function. It is known Anne and Oscar Lackner Chair in Medicine - controlling diaphragm function. It is known Anne and Oscar Lackner Chair in Medicine from experimental studies using a lateral C2 (PJR) and the Paralyzed Veterans of America from experimental studies using a lateral C2 (PJR) and the Paralyzed Veterans of America from experimental studies using a lateral C2 (PJR) and the Paralyzed Veterans of America hemisection (C2Hx) in the adult rat, however, (MAL). hemisection (C2Hx) in the adult rat, however, (MAL). hemisection (C2Hx) in the adult rat, however, (MAL). that spontaneous recovery of diaphragm that spontaneous recovery of diaphragm that spontaneous recovery of diaphragm function can occur. Recent experiments have P-42 High Cervical Spinal Cord Injury function can occur. Recent experiments have P-42 High Cervical Spinal Cord Injury function can occur. Recent experiments have P-42 High Cervical Spinal Cord Injury identified cervical interneurons that could Results In Altered Distributions of Medullary identified cervical interneurons that could Results In Altered Distributions of Medullary identified cervical interneurons that could Results In Altered Distributions of Medullary contribute to respiratory neuroplasticity Inspiratory And Expiratory Neuronal contribute to respiratory neuroplasticity Inspiratory And Expiratory Neuronal contribute to respiratory neuroplasticity Inspiratory And Expiratory Neuronal following lateralized hemisection lesions at C2 Activity following lateralized hemisection lesions at C2 Activity following lateralized hemisection lesions at C2 Activity (i.e., C2Hx). However, the activity of these (i.e., C2Hx). However, the activity of these (i.e., C2Hx). However, the activity of these putative pre-phrenic interneurons following L.M. Mercier1, D.F. Ryczek1, K-Z Lee2, B.E. putative pre-phrenic interneurons following L.M. Mercier1, D.F. Ryczek1, K-Z Lee2, B.E. putative pre-phrenic interneurons following L.M. Mercier1, D.F. Ryczek1, K-Z Lee2, B.E. C2Hx is not well-defined. The present study O’Steen1, D.D. Fuller2, P.J. Reier1, M.A. Lane C2Hx is not well-defined. The present study O’Steen1, D.D. Fuller2, P.J. Reier1, M.A. Lane C2Hx is not well-defined. The present study O’Steen1, D.D. Fuller2, P.J. Reier1, M.A. Lane compared normal activity patterns of cervical Department of Neuroscience (College of compared normal activity patterns of cervical Department of Neuroscience (College of compared normal activity patterns of cervical Department of Neuroscience (College of interneurons and motoneurons versus those seen Medicine)1 and Department of Physical interneurons and motoneurons versus those seen Medicine)1 and Department of Physical interneurons and motoneurons versus those seen Medicine)1 and Department of Physical under conditions of increased respiratory drive Therapy2 (College of Public Health and Health under conditions of increased respiratory drive Therapy2 (College of Public Health and Health under conditions of increased respiratory drive Therapy2 (College of Public Health and Health and/or following C2Hx. Adult female rats were Professions), University of Florida, Gainesville, and/or following C2Hx. Adult female rats were Professions), University of Florida, Gainesville, and/or following C2Hx. Adult female rats were Professions), University of Florida, Gainesville, divided into uninjured or C2Hx groups. Animals FL. divided into uninjured or C2Hx groups. Animals FL. divided into uninjured or C2Hx groups. Animals FL. were then allowed to recover for 2 weeks post- were then allowed to recover for 2 weeks post- were then allowed to recover for 2 weeks post- injury. Uninjured animals were euthanized Respiratory rhythm originates in the injury. Uninjured animals were euthanized Respiratory rhythm originates in the injury. Uninjured animals were euthanized Respiratory rhythm originates in the without experiencing any additional procedures medullary rostral and caudal ventral respiratory without experiencing any additional procedures medullary rostral and caudal ventral respiratory without experiencing any additional procedures medullary rostral and caudal ventral respiratory or following respiratory challenge (10 minute column (rVRC/cVRC) neurons, which extend or following respiratory challenge (10 minute column (rVRC/cVRC) neurons, which extend or following respiratory challenge (10 minute column (rVRC/cVRC) neurons, which extend

60 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 60 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 60 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE axonal projections to spinal neurons controlling ventilatory behavior, as well as compensation in axonal projections to spinal neurons controlling ventilatory behavior, as well as compensation in axonal projections to spinal neurons controlling ventilatory behavior, as well as compensation in inspiratory and expiratory muscle activity. spinal respiratory motor function. inspiratory and expiratory muscle activity. spinal respiratory motor function. inspiratory and expiratory muscle activity. spinal respiratory motor function. Interruption of those bulbospinal pathways Supported by: Paralyzed Veterans of America Interruption of those bulbospinal pathways Supported by: Paralyzed Veterans of America Interruption of those bulbospinal pathways Supported by: Paralyzed Veterans of America results in altered patterns of ventilation. While (MAL), NIH RO1 NS054025 and the Anne and results in altered patterns of ventilation. While (MAL), NIH RO1 NS054025 and the Anne and results in altered patterns of ventilation. While (MAL), NIH RO1 NS054025 and the Anne and various neuroplastic changes have been shown Oscar Lackner Chair in Medicine (PJR). various neuroplastic changes have been shown Oscar Lackner Chair in Medicine (PJR). various neuroplastic changes have been shown Oscar Lackner Chair in Medicine (PJR). in spinal respiratory centers following cervical in spinal respiratory centers following cervical in spinal respiratory centers following cervical spinal cord injury (SCI), it is unknown whether P-43 Synaptic Integration of Transplanted spinal cord injury (SCI), it is unknown whether P-43 Synaptic Integration of Transplanted spinal cord injury (SCI), it is unknown whether P-43 Synaptic Integration of Transplanted medullary respiratory circuitry is also affected. Cells With Phrenic Circuitry Following High medullary respiratory circuitry is also affected. Cells With Phrenic Circuitry Following High medullary respiratory circuitry is also affected. Cells With Phrenic Circuitry Following High Since supraspinal functional map changes have Cervical Spinal Cord Injury In Adult Rat Since supraspinal functional map changes have Cervical Spinal Cord Injury In Adult Rat Since supraspinal functional map changes have Cervical Spinal Cord Injury In Adult Rat been reported in other motor systems following been reported in other motor systems following been reported in other motor systems following SCI, we tested the hypothesis that a high C. Lopez1, J. Loftus1, E.J. Gonzalez-Rothi2, L.M. SCI, we tested the hypothesis that a high C. Lopez1, J. Loftus1, E.J. Gonzalez-Rothi2, L.M. SCI, we tested the hypothesis that a high C. Lopez1, J. Loftus1, E.J. Gonzalez-Rothi2, L.M. cervical lateralized hemisection (C2Hx) will Mercier1, A.M. Rombola1, B.E. O’Steen1, D.D. cervical lateralized hemisection (C2Hx) will Mercier1, A.M. Rombola1, B.E. O’Steen1, D.D. cervical lateralized hemisection (C2Hx) will Mercier1, A.M. Rombola1, B.E. O’Steen1, D.D. alter representation of brainstem respiratory Fuller2, M.A. Lane1, P.J. Reier1 alter representation of brainstem respiratory Fuller2, M.A. Lane1, P.J. Reier1 alter representation of brainstem respiratory Fuller2, M.A. Lane1, P.J. Reier1 neuronal activity. Departments of Neuroscience, College neuronal activity. Departments of Neuroscience, College neuronal activity. Departments of Neuroscience, College Adult, female rats received C2Hx, and at of Medicine1 and Physical Therapy, College of Adult, female rats received C2Hx, and at of Medicine1 and Physical Therapy, College of Adult, female rats received C2Hx, and at of Medicine1 and Physical Therapy, College of 2 or 12 weeks post-injury, electrophysiological Public Health and Health Professions2, 2 or 12 weeks post-injury, electrophysiological Public Health and Health Professions2, 2 or 12 weeks post-injury, electrophysiological Public Health and Health Professions2, mapping was performed of medullary neurons University of Florida, Gainesville, FL. 32610 mapping was performed of medullary neurons University of Florida, Gainesville, FL. 32610 mapping was performed of medullary neurons University of Florida, Gainesville, FL. 32610 active during breathing. Electrodes were active during breathing. Electrodes were active during breathing. Electrodes were inserted into multiple VRC locations (spaced Cervical spinal cord injuries frequently inserted into multiple VRC locations (spaced Cervical spinal cord injuries frequently inserted into multiple VRC locations (spaced Cervical spinal cord injuries frequently 200m, and at depths ~500m apart) to result in life-threatening respiratory dysfunction 200m, and at depths ~500m apart) to result in life-threatening respiratory dysfunction 200m, and at depths ~500m apart) to result in life-threatening respiratory dysfunction determine the respiratory activity, inspiratory or even at chronic post-injury times. Injuries determine the respiratory activity, inspiratory or even at chronic post-injury times. Injuries determine the respiratory activity, inspiratory or even at chronic post-injury times. Injuries expiratory, at each site ipsilateral to the C2Hx. rostral to C3-5 are especially devastating due to expiratory, at each site ipsilateral to the C2Hx. rostral to C3-5 are especially devastating due to expiratory, at each site ipsilateral to the C2Hx. rostral to C3-5 are especially devastating due to External intercostal EMG recordings obtained loss of bulbospinal inspiratory input to phrenic External intercostal EMG recordings obtained loss of bulbospinal inspiratory input to phrenic External intercostal EMG recordings obtained loss of bulbospinal inspiratory input to phrenic simultaneously defined the pattern of inspiratory motoneurons (PhMNs), resulting in severe simultaneously defined the pattern of inspiratory motoneurons (PhMNs), resulting in severe simultaneously defined the pattern of inspiratory motoneurons (PhMNs), resulting in severe activity. Phasic respiratory activity was impairment of diaphragm function. activity. Phasic respiratory activity was impairment of diaphragm function. activity. Phasic respiratory activity was impairment of diaphragm function. confirmed audibly and by correlation with EMG Experimentally, this is best illustrated by a well- confirmed audibly and by correlation with EMG Experimentally, this is best illustrated by a well- confirmed audibly and by correlation with EMG Experimentally, this is best illustrated by a well- signals. Maps from C2Hx animals were established lateralized C2 spinal hemisection signals. Maps from C2Hx animals were established lateralized C2 spinal hemisection signals. Maps from C2Hx animals were established lateralized C2 spinal hemisection compared to those obtained from spinal-intact (C2Hx) model in which injury results in compared to those obtained from spinal-intact (C2Hx) model in which injury results in compared to those obtained from spinal-intact (C2Hx) model in which injury results in rats. paralysis of the ipsilateral hemidiaphragm. rats. paralysis of the ipsilateral hemidiaphragm. rats. paralysis of the ipsilateral hemidiaphragm. In naïve rats, inspiratory activity occurs While some spontaneous diaphragm recovery In naïve rats, inspiratory activity occurs While some spontaneous diaphragm recovery In naïve rats, inspiratory activity occurs While some spontaneous diaphragm recovery predominantly in the rVRC, whereas expiratory has been demonstrated, the extent of predominantly in the rVRC, whereas expiratory has been demonstrated, the extent of predominantly in the rVRC, whereas expiratory has been demonstrated, the extent of activity is mostly present in the cVRC with each improvement remains limited. To determine activity is mostly present in the cVRC with each improvement remains limited. To determine activity is mostly present in the cVRC with each improvement remains limited. To determine partitioned by an intermediate zone of activity whether a cellular replacement approach can partitioned by an intermediate zone of activity whether a cellular replacement approach can partitioned by an intermediate zone of activity whether a cellular replacement approach can overlap. By 2 weeks post-injury, a dramatic enhance this neuroplastic outcome, we first overlap. By 2 weeks post-injury, a dramatic enhance this neuroplastic outcome, we first overlap. By 2 weeks post-injury, a dramatic enhance this neuroplastic outcome, we first reversal occurred in which inspiratory activity wished to determine whether donor neuronal reversal occurred in which inspiratory activity wished to determine whether donor neuronal reversal occurred in which inspiratory activity wished to determine whether donor neuronal recording sites were more frequently progenitors can become integrated with the recording sites were more frequently progenitors can become integrated with the recording sites were more frequently progenitors can become integrated with the represented caudally and expiratory activity phrenic circuitry and mediate improved represented caudally and expiratory activity phrenic circuitry and mediate improved represented caudally and expiratory activity phrenic circuitry and mediate improved sites increased rostrally. At 12 weeks post- ipsilateral hemidiaphragm function. sites increased rostrally. At 12 weeks post- ipsilateral hemidiaphragm function. sites increased rostrally. At 12 weeks post- ipsilateral hemidiaphragm function. injury, rostral expiratory activity expanded Accordingly, E13-14 rat fetal spinal cord tissue injury, rostral expiratory activity expanded Accordingly, E13-14 rat fetal spinal cord tissue injury, rostral expiratory activity expanded Accordingly, E13-14 rat fetal spinal cord tissue caudally with shrinking representation of was grafted into acute C2Hx lesions of adult, caudally with shrinking representation of was grafted into acute C2Hx lesions of adult, caudally with shrinking representation of was grafted into acute C2Hx lesions of adult, inspiratory activity in the cVRC. To our female Sprague-Dawley rats. Lesion-only inspiratory activity in the cVRC. To our female Sprague-Dawley rats. Lesion-only inspiratory activity in the cVRC. To our female Sprague-Dawley rats. Lesion-only knowledge, these electrophysiological data are animals served as controls. A retrograde knowledge, these electrophysiological data are animals served as controls. A retrograde knowledge, these electrophysiological data are animals served as controls. A retrograde the first demonstration of changes in neural transynaptic tracer – pseudorabies virus (PRV) – the first demonstration of changes in neural transynaptic tracer – pseudorabies virus (PRV) – the first demonstration of changes in neural transynaptic tracer – pseudorabies virus (PRV) – circuit phenotype associated with medullary was applied to the ipsilateral diaphragm or circuit phenotype associated with medullary was applied to the ipsilateral diaphragm or circuit phenotype associated with medullary was applied to the ipsilateral diaphragm or respiratory pattern generation following SCI. injected directly into transplanted tissue, to respiratory pattern generation following SCI. injected directly into transplanted tissue, to respiratory pattern generation following SCI. injected directly into transplanted tissue, to These findings may reflect changes in assess synaptic integration between the host These findings may reflect changes in assess synaptic integration between the host These findings may reflect changes in assess synaptic integration between the host

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 61 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 61 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 61 ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE neurons and transplanted cells. Terminal relevant contusion injuries at the level of the neurons and transplanted cells. Terminal relevant contusion injuries at the level of the neurons and transplanted cells. Terminal relevant contusion injuries at the level of the diaphragm EMG (DiaEMG) recordings were phrenic nucleus (C3-C5/6). The goal of the diaphragm EMG (DiaEMG) recordings were phrenic nucleus (C3-C5/6). The goal of the diaphragm EMG (DiaEMG) recordings were phrenic nucleus (C3-C5/6). The goal of the also obtained 24-72 hours after PRV delivery. present study was to define the extent of PhMN also obtained 24-72 hours after PRV delivery. present study was to define the extent of PhMN also obtained 24-72 hours after PRV delivery. present study was to define the extent of PhMN Recordings were made during eupneic breathing compromise following lateral mid-cervical Recordings were made during eupneic breathing compromise following lateral mid-cervical Recordings were made during eupneic breathing compromise following lateral mid-cervical (exposed to compressed air) or respiratory contusions and concomitant temporal changes in (exposed to compressed air) or respiratory contusions and concomitant temporal changes in (exposed to compressed air) or respiratory contusions and concomitant temporal changes in challenge (elicited by hypercapnia; 7% CO2 diaphragm EMG (diaEMG) activity and challenge (elicited by hypercapnia; 7% CO2 diaphragm EMG (diaEMG) activity and challenge (elicited by hypercapnia; 7% CO2 diaphragm EMG (diaEMG) activity and delivered via nose-cone). DiaEMG in untreated ventilatory function. Telemetric electrodes were delivered via nose-cone). DiaEMG in untreated ventilatory function. Telemetric electrodes were delivered via nose-cone). DiaEMG in untreated ventilatory function. Telemetric electrodes were animals revealed only limited activity bilaterally implanted in the diaphragms of adult animals revealed only limited activity bilaterally implanted in the diaphragms of adult animals revealed only limited activity bilaterally implanted in the diaphragms of adult ipsilateral, to C2Hx. Hypercapnia increased female rats. One week later, all animals received ipsilateral, to C2Hx. Hypercapnia increased female rats. One week later, all animals received ipsilateral, to C2Hx. Hypercapnia increased female rats. One week later, all animals received diaphragm activity, but ipsilateral output a C3/4 contusion (Infinite Horizon, 150kD diaphragm activity, but ipsilateral output a C3/4 contusion (Infinite Horizon, 150kD diaphragm activity, but ipsilateral output a C3/4 contusion (Infinite Horizon, 150kD remained impaired. In contrast, transplant present force). Diaphragm EMG recordings remained impaired. In contrast, transplant present force). Diaphragm EMG recordings remained impaired. In contrast, transplant present force). Diaphragm EMG recordings recipients showed improved muscle activity were made simultaneously with ventilatory recipients showed improved muscle activity were made simultaneously with ventilatory recipients showed improved muscle activity were made simultaneously with ventilatory ipsilateral to injury during eupneic and assessment (using whole-body ipsilateral to injury during eupneic and assessment (using whole-body ipsilateral to injury during eupneic and assessment (using whole-body challenged breathing. PRV tracing revealed plethysmography) in awake unanesthetized challenged breathing. PRV tracing revealed plethysmography) in awake unanesthetized challenged breathing. PRV tracing revealed plethysmography) in awake unanesthetized connectivity between donor neurons and the animals. Measurements were made pre-injury, connectivity between donor neurons and the animals. Measurements were made pre-injury, connectivity between donor neurons and the animals. Measurements were made pre-injury, host phrenic circuitry ipsilateral to injury. PRV daily during the first week post-injury, and host phrenic circuitry ipsilateral to injury. PRV daily during the first week post-injury, and host phrenic circuitry ipsilateral to injury. PRV daily during the first week post-injury, and injection into transplanted tissue revealed weekly thereafter while animals were exposed injection into transplanted tissue revealed weekly thereafter while animals were exposed injection into transplanted tissue revealed weekly thereafter while animals were exposed integration between donor neurons and 1) host to either normal (normoxic, normocapnic) or integration between donor neurons and 1) host to either normal (normoxic, normocapnic) or integration between donor neurons and 1) host to either normal (normoxic, normocapnic) or spinal interneurons in surrounding gray matter hypercapnic (7% CO2) air. Initial results spinal interneurons in surrounding gray matter hypercapnic (7% CO2) air. Initial results spinal interneurons in surrounding gray matter hypercapnic (7% CO2) air. Initial results and 2) medullary neurons in the ventral demonstrate the feasibility of long-term and 2) medullary neurons in the ventral demonstrate the feasibility of long-term and 2) medullary neurons in the ventral demonstrate the feasibility of long-term respiratory column, raphe and reticular nuclei. telemetric recordings of diaEMG activity. respiratory column, raphe and reticular nuclei. telemetric recordings of diaEMG activity. respiratory column, raphe and reticular nuclei. telemetric recordings of diaEMG activity. These results provide evidence for graft- Within the first two post-injury days, diaphragm These results provide evidence for graft- Within the first two post-injury days, diaphragm These results provide evidence for graft- Within the first two post-injury days, diaphragm mediated enhancement of post-C2Hx diaEMG activity increases while ventilation is relatively mediated enhancement of post-C2Hx diaEMG activity increases while ventilation is relatively mediated enhancement of post-C2Hx diaEMG activity increases while ventilation is relatively activity that may involve a host-graft unaffected. Furthermore, diaphragm activity and activity that may involve a host-graft unaffected. Furthermore, diaphragm activity and activity that may involve a host-graft unaffected. Furthermore, diaphragm activity and interneuronal relay. overall ventilatory responses to respiratory interneuronal relay. overall ventilatory responses to respiratory interneuronal relay. overall ventilatory responses to respiratory Supported by: NIH RO1 NS054025 (PJR) and challenge (hypercapnia) are dramatically Supported by: NIH RO1 NS054025 (PJR) and challenge (hypercapnia) are dramatically Supported by: NIH RO1 NS054025 (PJR) and challenge (hypercapnia) are dramatically the Anne and Oscar Lackner Chair in Medicine attenuated compared with that seen pre-injury. the Anne and Oscar Lackner Chair in Medicine attenuated compared with that seen pre-injury. the Anne and Oscar Lackner Chair in Medicine attenuated compared with that seen pre-injury. By 1 week post-injury, the ventilatory response By 1 week post-injury, the ventilatory response By 1 week post-injury, the ventilatory response P-44 Persistent Diaphragm Dysfunction to challenge normalizes. Although there is some P-44 Persistent Diaphragm Dysfunction to challenge normalizes. Although there is some P-44 Persistent Diaphragm Dysfunction to challenge normalizes. Although there is some Following Lateralized Cervical Contusion recovery of diaEMG responses to challenge, the Following Lateralized Cervical Contusion recovery of diaEMG responses to challenge, the Following Lateralized Cervical Contusion recovery of diaEMG responses to challenge, the extent remains significantly reduced relative to extent remains significantly reduced relative to extent remains significantly reduced relative to S. Hussey1, D.E. Sanchez1, B.E Osteen1, D.D. what occurs pre-injury. This deficit remains S. Hussey1, D.E. Sanchez1, B.E Osteen1, D.D. what occurs pre-injury. This deficit remains S. Hussey1, D.E. Sanchez1, B.E Osteen1, D.D. what occurs pre-injury. This deficit remains Fuller2, M.A. Lane1, P.J Reier1 persistent at 4 weeks post-injury. Persistent Fuller2, M.A. Lane1, P.J Reier1 persistent at 4 weeks post-injury. Persistent Fuller2, M.A. Lane1, P.J Reier1 persistent at 4 weeks post-injury. Persistent Departments of Neuroscience1 and diaphragm dysfunction in the presence of Departments of Neuroscience1 and diaphragm dysfunction in the presence of Departments of Neuroscience1 and diaphragm dysfunction in the presence of Physical Therapy2, University of Florida otherwise normal ventilatory patterns suggests Physical Therapy2, University of Florida otherwise normal ventilatory patterns suggests Physical Therapy2, University of Florida otherwise normal ventilatory patterns suggests College of Medicine1 and College of Public significant compensation in other respiratory College of Medicine1 and College of Public significant compensation in other respiratory College of Medicine1 and College of Public significant compensation in other respiratory Health and Health Professions2, Gainesville, motor systems (e.g., intercostal circuitry). Health and Health Professions2, Gainesville, motor systems (e.g., intercostal circuitry). Health and Health Professions2, Gainesville, motor systems (e.g., intercostal circuitry). FL., 32611 Ongoing studies are quantifying PhMN primary FL., 32611 Ongoing studies are quantifying PhMN primary FL., 32611 Ongoing studies are quantifying PhMN primary and secondary loss and examining the and secondary loss and examining the and secondary loss and examining the Cervical spinal cord injury (SCI) relationship between motoneuron loss and Cervical spinal cord injury (SCI) relationship between motoneuron loss and Cervical spinal cord injury (SCI) relationship between motoneuron loss and compromises phrenic circuitry resulting in diaphragm dysfunction. compromises phrenic circuitry resulting in diaphragm dysfunction. compromises phrenic circuitry resulting in diaphragm dysfunction. diaphragm paresis or paralysis. While research Supported by: NIH RO1 NS054025 (PJR) and diaphragm paresis or paralysis. While research Supported by: NIH RO1 NS054025 (PJR) and diaphragm paresis or paralysis. While research Supported by: NIH RO1 NS054025 (PJR) and using a lateralized C2 hemisection model has the Anne and Oscar Lackner Chair in Medicine. using a lateralized C2 hemisection model has the Anne and Oscar Lackner Chair in Medicine. using a lateralized C2 hemisection model has the Anne and Oscar Lackner Chair in Medicine. revealed the potential for spontaneous recovery revealed the potential for spontaneous recovery revealed the potential for spontaneous recovery and anatomical plasticity, less is known about P-45 Chondroitinase ABC Treatment And and anatomical plasticity, less is known about P-45 Chondroitinase ABC Treatment And and anatomical plasticity, less is known about P-45 Chondroitinase ABC Treatment And respiratory plasticity following more clinically Modest Exposure To Intermittent Hypoxia respiratory plasticity following more clinically Modest Exposure To Intermittent Hypoxia respiratory plasticity following more clinically Modest Exposure To Intermittent Hypoxia

62 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 62 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 62 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE ABSTRACTS OF POSTER PRESENTATIONS - SESSION ONE

Here we show that this combination treatment Here we show that this combination treatment Here we show that this combination treatment Restores Hemidiaphragmatic Activity After Restores Hemidiaphragmatic Activity After Restores Hemidiaphragmatic Activity After of ChABC and modest IH exposure can induce of ChABC and modest IH exposure can induce of ChABC and modest IH exposure can induce Cervical Spinal Cord Injury Cervical Spinal Cord Injury Cervical Spinal Cord Injury robust respiratory motor function after C2H. robust respiratory motor function after C2H. robust respiratory motor function after C2H.

1,2 1 2 Animals that received IH, with no ChABC 1,2 1 2 Animals that received IH, with no ChABC 1,2 1 2 Animals that received IH, with no ChABC W.J. Alilain , M. Clark , J. Silver W.J. Alilain , M. Clark , J. Silver W.J. Alilain , M. Clark , J. Silver 1 displayed little to no recovery. Taken together, 1 displayed little to no recovery. Taken together, 1 displayed little to no recovery. Taken together, Department of Neurosciences, Department of Neurosciences, Department of Neurosciences, 2 these results show that ChABC treatment 2 these results show that ChABC treatment 2 these results show that ChABC treatment Metrohealth Medical Center; Department of Metrohealth Medical Center; Department of Metrohealth Medical Center; Department of combined with an IH regimen that is far more combined with an IH regimen that is far more combined with an IH regimen that is far more Neurosciences, Case Western Reserve Neurosciences, Case Western Reserve Neurosciences, Case Western Reserve tolerable to the animal can augment recovery of tolerable to the animal can augment recovery of tolerable to the animal can augment recovery of University School of Medicine, University School of Medicine, University School of Medicine, respiratory motor function after SCI. respiratory motor function after SCI. respiratory motor function after SCI. Cleveland, OH USA Cleveland, OH USA Cleveland, OH USA P-46 Ipsilateral Inspiratory Intercostal P-46 Ipsilateral Inspiratory Intercostal P-46 Ipsilateral Inspiratory Intercostal Most spinal cord injuries (SCI) occur at Muscle Activity After C2 Spinal Cord Most spinal cord injuries (SCI) occur at Muscle Activity After C2 Spinal Cord Most spinal cord injuries (SCI) occur at Muscle Activity After C2 Spinal Cord the cervical level. This is particularly Hemisection the cervical level. This is particularly Hemisection the cervical level. This is particularly Hemisection devastating because the phrenic motor neurons, devastating because the phrenic motor neurons, devastating because the phrenic motor neurons, which innervate the diaphragm, are located at M. B. Zimmer1, J. Grant2, A. Ayar2 and H. G. which innervate the diaphragm, are located at M. B. Zimmer1, J. Grant2, A. Ayar2 and H. G. which innervate the diaphragm, are located at M. B. Zimmer1, J. Grant2, A. Ayar2 and H. G. this level. As a result, those afflicted with a Goshgarian2 this level. As a result, those afflicted with a Goshgarian2 this level. As a result, those afflicted with a Goshgarian2 cervical SCI usually have complications in 1Ferris State University, Department of cervical SCI usually have complications in 1Ferris State University, Department of cervical SCI usually have complications in 1Ferris State University, Department of breathing and can be dependent on a mechanical Biological Sciences, 820 Campus Drive 2120 breathing and can be dependent on a mechanical Biological Sciences, 820 Campus Drive 2120 breathing and can be dependent on a mechanical Biological Sciences, 820 Campus Drive 2120 ventilator in order to survive, severely limiting ASC, Big Rapids, MI, 2Wayne State University, ventilator in order to survive, severely limiting ASC, Big Rapids, MI, 2Wayne State University, ventilator in order to survive, severely limiting ASC, Big Rapids, MI, 2Wayne State University, their quality of life. To study these Department of Anatomy and Cell Biology, 540 their quality of life. To study these Department of Anatomy and Cell Biology, 540 their quality of life. To study these Department of Anatomy and Cell Biology, 540 complications and ways to restore respiratory East Canfield, Detroit MI. complications and ways to restore respiratory East Canfield, Detroit MI. complications and ways to restore respiratory East Canfield, Detroit MI. motor activity, our laboratory utilizes the lateral motor activity, our laboratory utilizes the lateral motor activity, our laboratory utilizes the lateral C2 hemisection (C2H) model of SCI. C2H Upper cervical spinal cord hemisection C2 hemisection (C2H) model of SCI. C2H Upper cervical spinal cord hemisection C2 hemisection (C2H) model of SCI. C2H Upper cervical spinal cord hemisection severs the ipsilateral bulbospinal inputs to the (e.g., at C2) causes paralysis of the ipsilateral severs the ipsilateral bulbospinal inputs to the (e.g., at C2) causes paralysis of the ipsilateral severs the ipsilateral bulbospinal inputs to the (e.g., at C2) causes paralysis of the ipsilateral phrenic nucleus and paralyses the ipsilateral hemidiaphragm, however, the effect of C2 phrenic nucleus and paralyses the ipsilateral hemidiaphragm, however, the effect of C2 phrenic nucleus and paralyses the ipsilateral hemidiaphragm, however, the effect of C2 hemidiaphragm while sparing the crossed hemisection on the function of the intercostal hemidiaphragm while sparing the crossed hemisection on the function of the intercostal hemidiaphragm while sparing the crossed hemisection on the function of the intercostal phrenic pathway which, although latent, serves muscles is not known. We hypothesized that phrenic pathway which, although latent, serves muscles is not known. We hypothesized that phrenic pathway which, although latent, serves muscles is not known. We hypothesized that as a potential anatomical substratum for ipsilateral intercostal muscles would be as a potential anatomical substratum for ipsilateral intercostal muscles would be as a potential anatomical substratum for ipsilateral intercostal muscles would be respiratory plasticity. Additionally, acutely paralyzed after C2 hemisection and activity respiratory plasticity. Additionally, acutely paralyzed after C2 hemisection and activity respiratory plasticity. Additionally, acutely paralyzed after C2 hemisection and activity following C2H, there is a dramatic upregulation would return in a time-dependent fashion. following C2H, there is a dramatic upregulation would return in a time-dependent fashion. following C2H, there is a dramatic upregulation would return in a time-dependent fashion. of the chondroitin sulfate proteoglycan (CSPG) Female, Sprague Dawley rats were anesthetized of the chondroitin sulfate proteoglycan (CSPG) Female, Sprague Dawley rats were anesthetized of the chondroitin sulfate proteoglycan (CSPG) Female, Sprague Dawley rats were anesthetized containing perineuronal net (PNN) around the with urethane and inspiratory intercostal EMG containing perineuronal net (PNN) around the with urethane and inspiratory intercostal EMG containing perineuronal net (PNN) around the with urethane and inspiratory intercostal EMG ipsilateral phrenic motor neurons. CSPGs and activity was recorded in control rats, acutely- ipsilateral phrenic motor neurons. CSPGs and activity was recorded in control rats, acutely- ipsilateral phrenic motor neurons. CSPGs and activity was recorded in control rats, acutely- the PNN can severely inhibit plasticity and injured C2 hemisected rats, and at 1 and 16 the PNN can severely inhibit plasticity and injured C2 hemisected rats, and at 1 and 16 the PNN can severely inhibit plasticity and injured C2 hemisected rats, and at 1 and 16 axonal regeneration, and thereby the means to weeks post C2 hemisection. Bilateral recordings axonal regeneration, and thereby the means to weeks post C2 hemisection. Bilateral recordings axonal regeneration, and thereby the means to weeks post C2 hemisection. Bilateral recordings restore function. Chondroitinase ABC of intercostal EMG activity showed that restore function. Chondroitinase ABC of intercostal EMG activity showed that restore function. Chondroitinase ABC of intercostal EMG activity showed that (ChABC) can digest these inhibitory matrix inspiratory activity was reduced immediately (ChABC) can digest these inhibitory matrix inspiratory activity was reduced immediately (ChABC) can digest these inhibitory matrix inspiratory activity was reduced immediately molecules and we have shown that with enzyme after injury and increased over time. EMG molecules and we have shown that with enzyme after injury and increased over time. EMG molecules and we have shown that with enzyme after injury and increased over time. EMG administration alone, there is a modest return of activity was observed first in rostral spaces administration alone, there is a modest return of activity was observed first in rostral spaces administration alone, there is a modest return of activity was observed first in rostral spaces hemidiaphragm activity after C2H. In other followed by recovery occurring in caudal hemidiaphragm activity after C2H. In other followed by recovery occurring in caudal hemidiaphragm activity after C2H. In other followed by recovery occurring in caudal models of SCI, combining ChABC treatment spaces. Theophylline increased respiratory models of SCI, combining ChABC treatment spaces. Theophylline increased respiratory models of SCI, combining ChABC treatment spaces. Theophylline increased respiratory with task-specific training can profoundly drive and increased intercostal activity; in some with task-specific training can profoundly drive and increased intercostal activity; in some with task-specific training can profoundly drive and increased intercostal activity; in some improve limb function. In the present study we cases inducing activity that was previously improve limb function. In the present study we cases inducing activity that was previously improve limb function. In the present study we cases inducing activity that was previously hypothesized that combining ChABC treatment absent. These results suggest for the first time hypothesized that combining ChABC treatment absent. These results suggest for the first time hypothesized that combining ChABC treatment absent. These results suggest for the first time with a very modest exposure to intermittent that there are crossed, initially latent, respiratory with a very modest exposure to intermittent that there are crossed, initially latent, respiratory with a very modest exposure to intermittent that there are crossed, initially latent, respiratory hypoxia (IH), which can strongly drive connections to neurons innervating the hypoxia (IH), which can strongly drive connections to neurons innervating the hypoxia (IH), which can strongly drive connections to neurons innervating the respiratory motor plasticity (at higher exposure intercostal muscles similar to those innervating respiratory motor plasticity (at higher exposure intercostal muscles similar to those innervating respiratory motor plasticity (at higher exposure intercostal muscles similar to those innervating times), will further promote breathing recovery. phrenic motor neurons. times), will further promote breathing recovery. phrenic motor neurons. times), will further promote breathing recovery. phrenic motor neurons.

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 63 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 63 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 63 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

P-47 Generation of High Purity Neuronal fibroblasts (Yamanaka-iPS-414C, Yamanaka- P-47 Generation of High Purity Neuronal fibroblasts (Yamanaka-iPS-414C, Yamanaka- P-47 Generation of High Purity Neuronal fibroblasts (Yamanaka-iPS-414C, Yamanaka- Progenitor Cells And Oligodendrocyte iPS-201B7, and Okano-iPS-WA29) were Progenitor Cells And Oligodendrocyte iPS-201B7, and Okano-iPS-WA29) were Progenitor Cells And Oligodendrocyte iPS-201B7, and Okano-iPS-WA29) were Progenitor Cells From Blastocyst-Derived exposed to identical expansion conditions Progenitor Cells From Blastocyst-Derived exposed to identical expansion conditions Progenitor Cells From Blastocyst-Derived exposed to identical expansion conditions Human Embryonic Stem Cells And Human followed by differentiation into neuronal and Human Embryonic Stem Cells And Human followed by differentiation into neuronal and Human Embryonic Stem Cells And Human followed by differentiation into neuronal and Induced Pluripotent Stem Cells oligodendrocyte progenitor cells. Proliferation Induced Pluripotent Stem Cells oligodendrocyte progenitor cells. Proliferation Induced Pluripotent Stem Cells oligodendrocyte progenitor cells. Proliferation rates and gross morphology were recorded rates and gross morphology were recorded rates and gross morphology were recorded M. Wedemeyer*1,2,3, K. Stahl*5, D. during expansion. During stem cell expansion, M. Wedemeyer*1,2,3, K. Stahl*5, D. during expansion. During stem cell expansion, M. Wedemeyer*1,2,3, K. Stahl*5, D. during expansion. During stem cell expansion, Ferguson1,2,3, J. Frame1,2,3, C. Cruz1,2,3, J. all lines had similar rates of proliferation and Ferguson1,2,3, J. Frame1,2,3, C. Cruz1,2,3, J. all lines had similar rates of proliferation and Ferguson1,2,3, J. Frame1,2,3, C. Cruz1,2,3, J. all lines had similar rates of proliferation and Harness1,2,3, G. Nistor5, H. Okano7, S. gross morphology. Yield and purity of Harness1,2,3, G. Nistor5, H. Okano7, S. gross morphology. Yield and purity of Harness1,2,3, G. Nistor5, H. Okano7, S. gross morphology. Yield and purity of Yamanaka6, H. Keirstead1,2,3,4,5 differentiated products were determined via cell Yamanaka6, H. Keirstead1,2,3,4,5 differentiated products were determined via cell Yamanaka6, H. Keirstead1,2,3,4,5 differentiated products were determined via cell * Both authors contributed equally to this work. counts and ICC profiling. ICC profiling * Both authors contributed equally to this work. counts and ICC profiling. ICC profiling * Both authors contributed equally to this work. counts and ICC profiling. ICC profiling 1 Department of Anatomy & indicated that both hESC lines and two of the 1 Department of Anatomy & indicated that both hESC lines and two of the 1 Department of Anatomy & indicated that both hESC lines and two of the Neurobiology, University of California Irvine; three hiPSC lines produced differentiated Neurobiology, University of California Irvine; three hiPSC lines produced differentiated Neurobiology, University of California Irvine; three hiPSC lines produced differentiated Irvine, CA, USA; 2Reeve Irvine Research products with a low percentage of Irvine, CA, USA; 2Reeve Irvine Research products with a low percentage of Irvine, CA, USA; 2Reeve Irvine Research products with a low percentage of Center, University of California Irvine; Irvine, contaminating cell populations. These two iPS Center, University of California Irvine; Irvine, contaminating cell populations. These two iPS Center, University of California Irvine; Irvine, contaminating cell populations. These two iPS CA, USA; 3Sue and Bill Gross Stem Cell lines matured faster than the hESCs. The third CA, USA; 3Sue and Bill Gross Stem Cell lines matured faster than the hESCs. The third CA, USA; 3Sue and Bill Gross Stem Cell lines matured faster than the hESCs. The third Research Center, University of California iPS line produced a very low yield of Research Center, University of California iPS line produced a very low yield of Research Center, University of California iPS line produced a very low yield of Irvine; Irvine, CA, USA; 4 Department of differentiated product, consisting primarily of Irvine; Irvine, CA, USA; 4 Department of differentiated product, consisting primarily of Irvine; Irvine, CA, USA; 4 Department of differentiated product, consisting primarily of Neurosurgery, University of California Irvine; undifferentiated neural cells. Despite the Neurosurgery, University of California Irvine; undifferentiated neural cells. Despite the Neurosurgery, University of California Irvine; undifferentiated neural cells. Despite the Irvine, CA, USA; 5California Stem Cell, Irvine, recently published differences between hiPSCs Irvine, CA, USA; 5California Stem Cell, Irvine, recently published differences between hiPSCs Irvine, CA, USA; 5California Stem Cell, Irvine, recently published differences between hiPSCs CA, USA; 5Center for Molecular Biology and and hESCs, properly screened iPS lines are CA, USA; 5Center for Molecular Biology and and hESCs, properly screened iPS lines are CA, USA; 5Center for Molecular Biology and and hESCs, properly screened iPS lines are Neuroscience, Department of Anatomy, Institute capable of producing differentiated products of Neuroscience, Department of Anatomy, Institute capable of producing differentiated products of Neuroscience, Department of Anatomy, Institute capable of producing differentiated products of of Basic Medical Science, University of Oslo; purity sufficient for clinical applications and of Basic Medical Science, University of Oslo; purity sufficient for clinical applications and of Basic Medical Science, University of Oslo; purity sufficient for clinical applications and Oslo, Norway; 6Center for iPS Research and should be tested in vivo to determine if Oslo, Norway; 6Center for iPS Research and should be tested in vivo to determine if Oslo, Norway; 6Center for iPS Research and should be tested in vivo to determine if Application, Kyoto University, Kyoto, Japan; differentiated products have functional Application, Kyoto University, Kyoto, Japan; differentiated products have functional Application, Kyoto University, Kyoto, Japan; differentiated products have functional 7Department of Physiology, School of Medicine, equivalence to those produced from hESC lines. 7Department of Physiology, School of Medicine, equivalence to those produced from hESC lines. 7Department of Physiology, School of Medicine, equivalence to those produced from hESC lines. Keio University, Tokyo, Japan Keio University, Tokyo, Japan Keio University, Tokyo, Japan P-48 Characterization Of High Purity P-48 Characterization Of High Purity P-48 Characterization Of High Purity The discovery that human somatic cells Neuronal Progenitors Isolated From Human The discovery that human somatic cells Neuronal Progenitors Isolated From Human The discovery that human somatic cells Neuronal Progenitors Isolated From Human can be reprogrammed to induced pluripotent Embryonic Stem Cells can be reprogrammed to induced pluripotent Embryonic Stem Cells can be reprogrammed to induced pluripotent Embryonic Stem Cells stem cells (hiPSCs) which closely resemble stem cells (hiPSCs) which closely resemble stem cells (hiPSCs) which closely resemble human embryonic stem cells (hESCs) garnered G Nistor2, A Poole2, M Siegenthaler2, J Sharp2, human embryonic stem cells (hESCs) garnered G Nistor2, A Poole2, M Siegenthaler2, J Sharp2, human embryonic stem cells (hESCs) garnered G Nistor2, A Poole2, M Siegenthaler2, J Sharp2, tremendous excitement. While iPS lines pass C Fredrickson2, C Airriess2, H Keirstead1 tremendous excitement. While iPS lines pass C Fredrickson2, C Airriess2, H Keirstead1 tremendous excitement. While iPS lines pass C Fredrickson2, C Airriess2, H Keirstead1 gross tests of pluripotency, more stringent 1 Reeve-Irvine Research Center, Sue and gross tests of pluripotency, more stringent 1 Reeve-Irvine Research Center, Sue and gross tests of pluripotency, more stringent 1 Reeve-Irvine Research Center, Sue and characterization indicates that most lines are Bill Gross Stem Cell Research Center, characterization indicates that most lines are Bill Gross Stem Cell Research Center, characterization indicates that most lines are Bill Gross Stem Cell Research Center, partially rather than completely reprogrammed. Department of Anatomy and Neurobiology, partially rather than completely reprogrammed. Department of Anatomy and Neurobiology, partially rather than completely reprogrammed. Department of Anatomy and Neurobiology, The objective of our work was to: 1) determine School of Medicine, Sue & Bill Gross Hall, a The objective of our work was to: 1) determine School of Medicine, Sue & Bill Gross Hall, a The objective of our work was to: 1) determine School of Medicine, Sue & Bill Gross Hall, a the degree of equivalence between three human CIRM Institute, University of California Irvine, the degree of equivalence between three human CIRM Institute, University of California Irvine, the degree of equivalence between three human CIRM Institute, University of California Irvine, iPS and two blastocyst-derived human ESC Irvine, California, United States of America; 2 iPS and two blastocyst-derived human ESC Irvine, California, United States of America; 2 iPS and two blastocyst-derived human ESC Irvine, California, United States of America; 2 lines and 2) determine whether differences have California Stem Cell, Inc., Irvine, California, lines and 2) determine whether differences have California Stem Cell, Inc., Irvine, California, lines and 2) determine whether differences have California Stem Cell, Inc., Irvine, California, functional implications for the ability of lines to United States of America functional implications for the ability of lines to United States of America functional implications for the ability of lines to United States of America produce neuronal and oligodendrocyte produce neuronal and oligodendrocyte produce neuronal and oligodendrocyte progenitor lines via clinically relevant high Human Neuronal Progenitors (hNPs) are progenitor lines via clinically relevant high Human Neuronal Progenitors (hNPs) are progenitor lines via clinically relevant high Human Neuronal Progenitors (hNPs) are purity differentiation protocols. Two blastocyst- difficult to obtain in large quantities from purity differentiation protocols. Two blastocyst- difficult to obtain in large quantities from purity differentiation protocols. Two blastocyst- difficult to obtain in large quantities from derived hESC lines (H7 and CSC-14) and three primary source. Neuronal Progenitors are more derived hESC lines (H7 and CSC-14) and three primary source. Neuronal Progenitors are more derived hESC lines (H7 and CSC-14) and three primary source. Neuronal Progenitors are more hiPSC lines derived from adult human dermal lineage-restrictive then Neural Progenitors, hiPSC lines derived from adult human dermal lineage-restrictive then Neural Progenitors, hiPSC lines derived from adult human dermal lineage-restrictive then Neural Progenitors,

64 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 64 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 64 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO since they do not differentiate into glial cells, neurodegenerative events in the human. Current since they do not differentiate into glial cells, neurodegenerative events in the human. Current since they do not differentiate into glial cells, neurodegenerative events in the human. Current but are rather committed to neuronal lineage. cellular models are complicated by primary but are rather committed to neuronal lineage. cellular models are complicated by primary but are rather committed to neuronal lineage. cellular models are complicated by primary The availability of hNPs in high purity would extraction and purification methods or are The availability of hNPs in high purity would extraction and purification methods or are The availability of hNPs in high purity would extraction and purification methods or are greatly facilitate neuronal drug discovery and confounded by contaminant progenitor greatly facilitate neuronal drug discovery and confounded by contaminant progenitor greatly facilitate neuronal drug discovery and confounded by contaminant progenitor developmental studies, as well as cell populations. The need exists for high purity developmental studies, as well as cell populations. The need exists for high purity developmental studies, as well as cell populations. The need exists for high purity replacement strategies for neurodegenerative MSN and lateral ganglionic eminence replacement strategies for neurodegenerative MSN and lateral ganglionic eminence replacement strategies for neurodegenerative MSN and lateral ganglionic eminence diseases and conditions. Here we describe a progenitors (LGP) at multiple developmental diseases and conditions. Here we describe a progenitors (LGP) at multiple developmental diseases and conditions. Here we describe a progenitors (LGP) at multiple developmental method for producing hNPs in large quantity stages for transplant studies as well as drug method for producing hNPs in large quantity stages for transplant studies as well as drug method for producing hNPs in large quantity stages for transplant studies as well as drug and high purity from human embryonic stem discovery and predictive toxicology assays. and high purity from human embryonic stem discovery and predictive toxicology assays. and high purity from human embryonic stem discovery and predictive toxicology assays. cells (hESCs) in a clinically compliant manner. Genetically abnormal blastocysts donated by cells (hESCs) in a clinically compliant manner. Genetically abnormal blastocysts donated by cells (hESCs) in a clinically compliant manner. Genetically abnormal blastocysts donated by The resulting population displays characteristic participants were thawed and an hESC line was The resulting population displays characteristic participants were thawed and an hESC line was The resulting population displays characteristic participants were thawed and an hESC line was neuronal-specific markers, such as nestin, Pax6 derived and maintained in animal-free neuronal-specific markers, such as nestin, Pax6 derived and maintained in animal-free neuronal-specific markers, such as nestin, Pax6 derived and maintained in animal-free and doublecortin. When allowed to conditions and characterized. hUCI-HD1 is a and doublecortin. When allowed to conditions and characterized. hUCI-HD1 is a and doublecortin. When allowed to conditions and characterized. hUCI-HD1 is a spontaneously differentiate into neuronal karyotypically normal HD line carrying 44 CAG spontaneously differentiate into neuronal karyotypically normal HD line carrying 44 CAG spontaneously differentiate into neuronal karyotypically normal HD line carrying 44 CAG subtypes in vitro, cholinergic, serotonergic, repeats. Undifferentiated hESC were grown on subtypes in vitro, cholinergic, serotonergic, repeats. Undifferentiated hESC were grown on subtypes in vitro, cholinergic, serotonergic, repeats. Undifferentiated hESC were grown on dopaminergic and/or noradrenergic, and matrigel-coated flasks to subconfluence in a dopaminergic and/or noradrenergic, and matrigel-coated flasks to subconfluence in a dopaminergic and/or noradrenergic, and matrigel-coated flasks to subconfluence in a medium spiny striatal neurons were observed. feeder-free system. Cultures were then medium spiny striatal neurons were observed. feeder-free system. Cultures were then medium spiny striatal neurons were observed. feeder-free system. Cultures were then When exposed to media known to promote the transitioned from conditioned medium to a When exposed to media known to promote the transitioned from conditioned medium to a When exposed to media known to promote the transitioned from conditioned medium to a propagation of glial cells, hNPs failed to form DMEM-F12 rich medium for neural induction. propagation of glial cells, hNPs failed to form DMEM-F12 rich medium for neural induction. propagation of glial cells, hNPs failed to form DMEM-F12 rich medium for neural induction. glial cells. These data demonstrate the lineage Cells were grown in suspension and passaged glial cells. These data demonstrate the lineage Cells were grown in suspension and passaged glial cells. These data demonstrate the lineage Cells were grown in suspension and passaged specificity of hNPs and their ability to produce a routinely in differentiation medium specificity of hNPs and their ability to produce a routinely in differentiation medium specificity of hNPs and their ability to produce a routinely in differentiation medium variety of different neuronal subtypes. supplemented with growth factors until day 60, variety of different neuronal subtypes. supplemented with growth factors until day 60, variety of different neuronal subtypes. supplemented with growth factors until day 60, when they were replated and growth factors when they were replated and growth factors when they were replated and growth factors P-49 Developing A Human Drug Discovery were withheld for final maturation to MSN by P-49 Developing A Human Drug Discovery were withheld for final maturation to MSN by P-49 Developing A Human Drug Discovery were withheld for final maturation to MSN by Platform For Huntington’s Disease day 66. Stage-specific immunocytochemistry Platform For Huntington’s Disease day 66. Stage-specific immunocytochemistry Platform For Huntington’s Disease day 66. Stage-specific immunocytochemistry was performed at day 14 (GSH-2), day 25, day was performed at day 14 (GSH-2), day 25, day was performed at day 14 (GSH-2), day 25, day J.V. Harness1,2,3,4, C. Armstrong3, M. Evans3, I. 42 and 45 (FoxP1) and day 66 (DARPP-32) to J.V. Harness1,2,3,4, C. Armstrong3, M. Evans3, I. 42 and 45 (FoxP1) and day 66 (DARPP-32) to J.V. Harness1,2,3,4, C. Armstrong3, M. Evans3, I. 42 and 45 (FoxP1) and day 66 (DARPP-32) to Soltesz3, L. Thompson2,5, H.S. Keirstead1,2,3,4 optimize growth conditions. Cultures were Soltesz3, L. Thompson2,5, H.S. Keirstead1,2,3,4 optimize growth conditions. Cultures were Soltesz3, L. Thompson2,5, H.S. Keirstead1,2,3,4 optimize growth conditions. Cultures were 1Reeve-Irvine Research Center, additionally matured to day 135 and 1Reeve-Irvine Research Center, additionally matured to day 135 and 1Reeve-Irvine Research Center, additionally matured to day 135 and University of California, Irvine, CA; 2Sue and electrophysiology was performed, University of California, Irvine, CA; 2Sue and electrophysiology was performed, University of California, Irvine, CA; 2Sue and electrophysiology was performed, Bill Gross Stem Cell Research Center, demonstrating neuronal firing patterns and Bill Gross Stem Cell Research Center, demonstrating neuronal firing patterns and Bill Gross Stem Cell Research Center, demonstrating neuronal firing patterns and University of California, Irvine, CA; 3Dept of functional synaptic connections. During University of California, Irvine, CA; 3Dept of functional synaptic connections. During University of California, Irvine, CA; 3Dept of functional synaptic connections. During Anatomy and Neurobiology, University of recording of spontaneous post-synaptic currents, Anatomy and Neurobiology, University of recording of spontaneous post-synaptic currents, Anatomy and Neurobiology, University of recording of spontaneous post-synaptic currents, California, Irvine, CA; 4Dept of Neurological NBQX/APV and GABAzine were used to block California, Irvine, CA; 4Dept of Neurological NBQX/APV and GABAzine were used to block California, Irvine, CA; 4Dept of Neurological NBQX/APV and GABAzine were used to block Surgery, University of California, Irvine, CA; glutamatergic and GABAergic events, showing Surgery, University of California, Irvine, CA; glutamatergic and GABAergic events, showing Surgery, University of California, Irvine, CA; glutamatergic and GABAergic events, showing 5Dept of Psychiatry and Human Behavior, that the cells received both excitatory and 5Dept of Psychiatry and Human Behavior, that the cells received both excitatory and 5Dept of Psychiatry and Human Behavior, that the cells received both excitatory and University of California, Irvine inhibitory inputs. The early stage LGP will be University of California, Irvine inhibitory inputs. The early stage LGP will be University of California, Irvine inhibitory inputs. The early stage LGP will be used for studies of striatal development and the used for studies of striatal development and the used for studies of striatal development and the The objective of this work is to develop MSN will be used for transplant studies, drug The objective of this work is to develop MSN will be used for transplant studies, drug The objective of this work is to develop MSN will be used for transplant studies, drug a high purity human stem cell based drug discovery and predictive toxicology. a high purity human stem cell based drug discovery and predictive toxicology. a high purity human stem cell based drug discovery and predictive toxicology. discovery platform for Huntington’s Disease discovery platform for Huntington’s Disease discovery platform for Huntington’s Disease (HD). HD is a neurodegenerative genetic P-50 High Purity Mouse Embryonic Stem (HD). HD is a neurodegenerative genetic P-50 High Purity Mouse Embryonic Stem (HD). HD is a neurodegenerative genetic P-50 High Purity Mouse Embryonic Stem disorder that results primarily in the loss of Cell-Derived Progenitor Motor Neurons For disorder that results primarily in the loss of Cell-Derived Progenitor Motor Neurons For disorder that results primarily in the loss of Cell-Derived Progenitor Motor Neurons For medium spiny projection neurons (MSN) of the Transplantation After Spinal Cord Injury medium spiny projection neurons (MSN) of the Transplantation After Spinal Cord Injury medium spiny projection neurons (MSN) of the Transplantation After Spinal Cord Injury striatum. Current animal models do not striatum. Current animal models do not striatum. Current animal models do not sufficiently recapitulate the complex cascade of sufficiently recapitulate the complex cascade of sufficiently recapitulate the complex cascade of

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 65 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 65 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 65 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

D.A. McCreedy1, C.R. Silverman1,2, D.I. analyzed using flow cytometry. Selection with D.A. McCreedy1, C.R. Silverman1,2, D.I. analyzed using flow cytometry. Selection with D.A. McCreedy1, C.R. Silverman1,2, D.I. analyzed using flow cytometry. Selection with Gottliebb2, S.E. Sakiyama-Elbert1 puromycin led to an approximately 2-fold Gottliebb2, S.E. Sakiyama-Elbert1 puromycin led to an approximately 2-fold Gottliebb2, S.E. Sakiyama-Elbert1 puromycin led to an approximately 2-fold 1Dept. of Biomedical Engineering, increase in the percentage of cells expressing 1Dept. of Biomedical Engineering, increase in the percentage of cells expressing 1Dept. of Biomedical Engineering, increase in the percentage of cells expressing Washington University in St. Louis, 1 Brookings Olig2. Similarly, the percentage of cells Washington University in St. Louis, 1 Brookings Olig2. Similarly, the percentage of cells Washington University in St. Louis, 1 Brookings Olig2. Similarly, the percentage of cells Dr. Box 1097, St. Louis, MO 63112; 2Dept. of expressing Hb9 was increased approximately 3- Dr. Box 1097, St. Louis, MO 63112; 2Dept. of expressing Hb9 was increased approximately 3- Dr. Box 1097, St. Louis, MO 63112; 2Dept. of expressing Hb9 was increased approximately 3- Anatomy and Neurobiology, Washington fold. These results demonstrate that transgenic Anatomy and Neurobiology, Washington fold. These results demonstrate that transgenic Anatomy and Neurobiology, Washington fold. These results demonstrate that transgenic University School of Medicine, Campus Box selection under Olig2 GREs can enrich cultures University School of Medicine, Campus Box selection under Olig2 GREs can enrich cultures University School of Medicine, Campus Box selection under Olig2 GREs can enrich cultures 8108, 660 South Euclid Avenue, St. Louis, MO for MNs and OPCs. 8108, 660 South Euclid Avenue, St. Louis, MO for MNs and OPCs. 8108, 660 South Euclid Avenue, St. Louis, MO for MNs and OPCs. 63110 References 63110 References 63110 References Keirstead HS et al. Human Embryonic Stem Cell-derived Keirstead HS et al. Human Embryonic Stem Cell-derived Keirstead HS et al. Human Embryonic Stem Cell-derived Oligodendrocyte Progenitor Cell Transplants Remyelinate Oligodendrocyte Progenitor Cell Transplants Remyelinate Oligodendrocyte Progenitor Cell Transplants Remyelinate Embryonic stem cell (ESC)-derived and Restore Locomotion after Spinal Cord Injury. J Embryonic stem cell (ESC)-derived and Restore Locomotion after Spinal Cord Injury. J Embryonic stem cell (ESC)-derived and Restore Locomotion after Spinal Cord Injury. J motoneurons (MNs) and ESC-derived Neurosci. 2005 May 11; 25 (19): 4694-705. motoneurons (MNs) and ESC-derived Neurosci. 2005 May 11; 25 (19): 4694-705. motoneurons (MNs) and ESC-derived Neurosci. 2005 May 11; 25 (19): 4694-705. oligodendrocyte precursor cells (OPCs) have oligodendrocyte precursor cells (OPCs) have oligodendrocyte precursor cells (OPCs) have been shown to have therapeutic potential in P-51 The Effects of Human Motor Neuron been shown to have therapeutic potential in P-51 The Effects of Human Motor Neuron been shown to have therapeutic potential in P-51 The Effects of Human Motor Neuron 1 1 1 preclinical models of spinal cord injury (SCI) . Progenitor Transplants In A Mouse Model preclinical models of spinal cord injury (SCI) . Progenitor Transplants In A Mouse Model preclinical models of spinal cord injury (SCI) . Progenitor Transplants In A Mouse Model Differentiation of ESCs into spinal MNs and Of Spinal Muscular Atrophy Differentiation of ESCs into spinal MNs and Of Spinal Muscular Atrophy Differentiation of ESCs into spinal MNs and Of Spinal Muscular Atrophy OPCs can be achieved in vitro following OPCs can be achieved in vitro following OPCs can be achieved in vitro following exposure to retinoic acid (RA) and sonic T.J. Wyatt1, S. Rossi1, G. Nistor1, A. Poole2, M. exposure to retinoic acid (RA) and sonic T.J. Wyatt1, S. Rossi1, G. Nistor1, A. Poole2, M. exposure to retinoic acid (RA) and sonic T.J. Wyatt1, S. Rossi1, G. Nistor1, A. Poole2, M. hedgehog (Shh); however, this results in low Siegenthaler2, H.S. Keirstead1 hedgehog (Shh); however, this results in low Siegenthaler2, H.S. Keirstead1 hedgehog (Shh); however, this results in low Siegenthaler2, H.S. Keirstead1 purity MN and OPC cultures. Current protocols 1Reeve-Irvine Research Center, Sue and purity MN and OPC cultures. Current protocols 1Reeve-Irvine Research Center, Sue and purity MN and OPC cultures. Current protocols 1Reeve-Irvine Research Center, Sue and to increase MN and OPC purity are lengthy and Bill Gross Stem Cell Research Center, to increase MN and OPC purity are lengthy and Bill Gross Stem Cell Research Center, to increase MN and OPC purity are lengthy and Bill Gross Stem Cell Research Center, technically challenging. In vivo, spinal cord Department of Anatomy & Neurobiology, technically challenging. In vivo, spinal cord Department of Anatomy & Neurobiology, technically challenging. In vivo, spinal cord Department of Anatomy & Neurobiology, MNs and some OPCs differentiate from School of Medicine, 1101 Gross Hall, MNs and some OPCs differentiate from School of Medicine, 1101 Gross Hall, MNs and some OPCs differentiate from School of Medicine, 1101 Gross Hall, progenitor motor neurons (pMN) in the ventral University of California at Irvine, Irvine, CA, progenitor motor neurons (pMN) in the ventral University of California at Irvine, Irvine, CA, progenitor motor neurons (pMN) in the ventral University of California at Irvine, Irvine, CA, neural tube, which express the transcription 92697-4292; 2California Stem Cell, Inc. 5251 neural tube, which express the transcription 92697-4292; 2California Stem Cell, Inc. 5251 neural tube, which express the transcription 92697-4292; 2California Stem Cell, Inc. 5251 factor Olig2. A subset of pMNs downregulate California Ave, Irvine, CA, 92612 factor Olig2. A subset of pMNs downregulate California Ave, Irvine, CA, 92612 factor Olig2. A subset of pMNs downregulate California Ave, Irvine, CA, 92612 Olig2 and commit to the MN fate, while others Olig2 and commit to the MN fate, while others Olig2 and commit to the MN fate, while others will maintain Olig2 expression and become Infantile spinal muscular atrophy (SMA) will maintain Olig2 expression and become Infantile spinal muscular atrophy (SMA) will maintain Olig2 expression and become Infantile spinal muscular atrophy (SMA) OPCs. Transgenic selection under control of the is the most common and severe hereditary OPCs. Transgenic selection under control of the is the most common and severe hereditary OPCs. Transgenic selection under control of the is the most common and severe hereditary Olig2 gene regulatory elements (GREs) may neurological disease in childhood, and is Olig2 gene regulatory elements (GREs) may neurological disease in childhood, and is Olig2 gene regulatory elements (GREs) may neurological disease in childhood, and is therefore provide a simple and inexpensive characterized by motor neuron loss. Children therefore provide a simple and inexpensive characterized by motor neuron loss. Children therefore provide a simple and inexpensive characterized by motor neuron loss. Children method to enrich cultures for MNs and OPCs. In diagnosed with SMA demonstrate severe method to enrich cultures for MNs and OPCs. In diagnosed with SMA demonstrate severe method to enrich cultures for MNs and OPCs. In diagnosed with SMA demonstrate severe this study, we generated a transgenic mouse ES muscle weakness that makes it difficult for them this study, we generated a transgenic mouse ES muscle weakness that makes it difficult for them this study, we generated a transgenic mouse ES muscle weakness that makes it difficult for them cell line (P-Olig2) that provides specific to breathe, eat, and move, and >95% die within cell line (P-Olig2) that provides specific to breathe, eat, and move, and >95% die within cell line (P-Olig2) that provides specific to breathe, eat, and move, and >95% die within resistance to the antibiotic puromycin under the 2 years. There is currently no treatment that can resistance to the antibiotic puromycin under the 2 years. There is currently no treatment that can resistance to the antibiotic puromycin under the 2 years. There is currently no treatment that can control of the Olig2 GREs. P-Olig2 ESCs were change the course of the disease. This study set control of the Olig2 GREs. P-Olig2 ESCs were change the course of the disease. This study set control of the Olig2 GREs. P-Olig2 ESCs were change the course of the disease. This study set exposed to retinoic acid and purmorphamine, a out to determine the histological, molecular, and exposed to retinoic acid and purmorphamine, a out to determine the histological, molecular, and exposed to retinoic acid and purmorphamine, a out to determine the histological, molecular, and - + - + - + Shh signalling agonist, using a 2 /4 induction functional effects following intraspinal Shh signalling agonist, using a 2 /4 induction functional effects following intraspinal Shh signalling agonist, using a 2 /4 induction functional effects following intraspinal protocol. First, ESCs were aggregated into transplantation of human embryonic stem cell- protocol. First, ESCs were aggregated into transplantation of human embryonic stem cell- protocol. First, ESCs were aggregated into transplantation of human embryonic stem cell- embryoid bodies (EBs) for two days in derived motor neuron progenitors (hESC- embryoid bodies (EBs) for two days in derived motor neuron progenitors (hESC- embryoid bodies (EBs) for two days in derived motor neuron progenitors (hESC- suspension culture then transferred to gelatin MNPs) into established models of 7SMA suspension culture then transferred to gelatin MNPs) into established models of 7SMA suspension culture then transferred to gelatin MNPs) into established models of 7SMA coated well plates and induced with 2 µM RA (SMNdelta7;SMN2;Smn-/-), and ALS (G93A coated well plates and induced with 2 µM RA (SMNdelta7;SMN2;Smn-/-), and ALS (G93A coated well plates and induced with 2 µM RA (SMNdelta7;SMN2;Smn-/-), and ALS (G93A and 1.5 µM purmorphamine for an additional SOD1) all of which are characterized by motor and 1.5 µM purmorphamine for an additional SOD1) all of which are characterized by motor and 1.5 µM purmorphamine for an additional SOD1) all of which are characterized by motor four days. Puromycin was added during the final neuron loss. hESC-MNPs were transplanted into four days. Puromycin was added during the final neuron loss. hESC-MNPs were transplanted into four days. Puromycin was added during the final neuron loss. hESC-MNPs were transplanted into two days for selection. Markers for pMNs/OPCs both models of motor neuron loss and their two days for selection. Markers for pMNs/OPCs both models of motor neuron loss and their two days for selection. Markers for pMNs/OPCs both models of motor neuron loss and their (Olig2) and newly committed MNs (Hb9) were migration, engraftment, differentiation and (Olig2) and newly committed MNs (Hb9) were migration, engraftment, differentiation and (Olig2) and newly committed MNs (Hb9) were migration, engraftment, differentiation and

66 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 66 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 66 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO repair potential within the diseased or injured SCRG and progenitors of the SVZ and CC is repair potential within the diseased or injured SCRG and progenitors of the SVZ and CC is repair potential within the diseased or injured SCRG and progenitors of the SVZ and CC is tissue was assessed. Our data demonstrates particularly enriched in genes associated with tissue was assessed. Our data demonstrates particularly enriched in genes associated with tissue was assessed. Our data demonstrates particularly enriched in genes associated with limited migration, stable engraftment, human disease. Visualizing SCRG in a FABP7- limited migration, stable engraftment, human disease. Visualizing SCRG in a FABP7- limited migration, stable engraftment, human disease. Visualizing SCRG in a FABP7- differentiation, sparing of endogenous tissue, GFP reporter mouse reveals an extensive differentiation, sparing of endogenous tissue, GFP reporter mouse reveals an extensive differentiation, sparing of endogenous tissue, GFP reporter mouse reveals an extensive and functional benefit as a result of population of SCRG that extend processes and functional benefit as a result of population of SCRG that extend processes and functional benefit as a result of population of SCRG that extend processes transplantation, likely as a result of growth linearly through the white matter (WM), around transplantation, likely as a result of growth linearly through the white matter (WM), around transplantation, likely as a result of growth linearly through the white matter (WM), around factor secretion. Currently, we are looking at the the SC boundary and inwardly towards the SC factor secretion. Currently, we are looking at the the SC boundary and inwardly towards the SC factor secretion. Currently, we are looking at the the SC boundary and inwardly towards the SC effect of hESC-MNP transplants on respiration gray matter, whose abundance increases in a effect of hESC-MNP transplants on respiration gray matter, whose abundance increases in a effect of hESC-MNP transplants on respiration gray matter, whose abundance increases in a and survival in 7SMA mice by transplanting in gradient from cervical to lumbar SC. Confocal and survival in 7SMA mice by transplanting in gradient from cervical to lumbar SC. Confocal and survival in 7SMA mice by transplanting in gradient from cervical to lumbar SC. Confocal the upper thoracic region of the spinal cord, in analysis of multiple NSC-enriched proteins the upper thoracic region of the spinal cord, in analysis of multiple NSC-enriched proteins the upper thoracic region of the spinal cord, in analysis of multiple NSC-enriched proteins addition to the normal lumbar transplantation reveals that postnatal SCRG are a discrete and addition to the normal lumbar transplantation reveals that postnatal SCRG are a discrete and addition to the normal lumbar transplantation reveals that postnatal SCRG are a discrete and site. hESC-MNPs represent a biological tool to heterogeneous potential progenitor population site. hESC-MNPs represent a biological tool to heterogeneous potential progenitor population site. hESC-MNPs represent a biological tool to heterogeneous potential progenitor population investigate human motor neuron development, distinct from white matter astrocytes. SCRG investigate human motor neuron development, distinct from white matter astrocytes. SCRG investigate human motor neuron development, distinct from white matter astrocytes. SCRG and provide a clinically relevant cell population become activated by multiple SC lesions, and, and provide a clinically relevant cell population become activated by multiple SC lesions, and, and provide a clinically relevant cell population become activated by multiple SC lesions, and, for the development of therapies to treat injuries like CC progenitors, are also more for the development of therapies to treat injuries like CC progenitors, are also more for the development of therapies to treat injuries like CC progenitors, are also more or diseases characterized by motor neuron loss. heterogeneous than previously appreciated. or diseases characterized by motor neuron loss. heterogeneous than previously appreciated. or diseases characterized by motor neuron loss. heterogeneous than previously appreciated. Gene ontology analysis highlights potentially Gene ontology analysis highlights potentially Gene ontology analysis highlights potentially P-52 Adult Spinal Cord Radial Glia unique regulatory pathways that may be further P-52 Adult Spinal Cord Radial Glia unique regulatory pathways that may be further P-52 Adult Spinal Cord Radial Glia unique regulatory pathways that may be further Display A Unique Progenitor Phenotype manipulated in SCRG to enhance repair in the Display A Unique Progenitor Phenotype manipulated in SCRG to enhance repair in the Display A Unique Progenitor Phenotype manipulated in SCRG to enhance repair in the A. Petit1, A. D. Sanders1, T. E. Kennedy2, W. context of SC injury and disease. A. Petit1, A. D. Sanders1, T. E. Kennedy2, W. context of SC injury and disease. A. Petit1, A. D. Sanders1, T. E. Kennedy2, W. context of SC injury and disease. Tetzlaff1, K. J. Glattfelder3, R. A. Dalley3, R. B. Tetzlaff1, K. J. Glattfelder3, R. A. Dalley3, R. B. Tetzlaff1, K. J. Glattfelder3, R. A. Dalley3, R. B. Puchalski3, A. R. Jones3, **A. J. Roskams1 P-53 Anatomical & Functional Puchalski3, A. R. Jones3, **A. J. Roskams1 P-53 Anatomical & Functional Puchalski3, A. R. Jones3, **A. J. Roskams1 P-53 Anatomical & Functional 1Dept. of Zoology; Life Sciences Institute Characterization Of Fenestrated 1Dept. of Zoology; Life Sciences Institute Characterization Of Fenestrated 1Dept. of Zoology; Life Sciences Institute Characterization Of Fenestrated and iCORD, University of British Columbia; Endothelium Formation During and iCORD, University of British Columbia; Endothelium Formation During and iCORD, University of British Columbia; Endothelium Formation During Vancouver, BC, V6T 1Z3, Canada; 2Dept. of Revascularization In The Injured Spinal Vancouver, BC, V6T 1Z3, Canada; 2Dept. of Revascularization In The Injured Spinal Vancouver, BC, V6T 1Z3, Canada; 2Dept. of Revascularization In The Injured Spinal Neurology and Neurosurgery; Montreal Cord Neurology and Neurosurgery; Montreal Cord Neurology and Neurosurgery; Montreal Cord Neurological Institute, McGill University; Neurological Institute, McGill University; Neurological Institute, McGill University; Montreal, Qc, H3A 2B4, Canada; 3Allen A.P. Montague1,4 , A. Ribble 1,2, C. Conrad 1,2, Montreal, Qc, H3A 2B4, Canada; 3Allen A.P. Montague1,4 , A. Ribble 1,2, C. Conrad 1,2, Montreal, Qc, H3A 2B4, Canada; 3Allen A.P. Montague1,4 , A. Ribble 1,2, C. Conrad 1,2, Institute for Brain Science; Seattle, WA, 98103, A.B. Mozer1,2, and R.L. Benton 1,2,3. Institute for Brain Science; Seattle, WA, 98103, A.B. Mozer1,2, and R.L. Benton 1,2,3. Institute for Brain Science; Seattle, WA, 98103, A.B. Mozer1,2, and R.L. Benton 1,2,3. USA 1Kentucky Spinal Cord Injury Research USA 1Kentucky Spinal Cord Injury Research USA 1Kentucky Spinal Cord Injury Research Center (KSCIRC) and Departments of Center (KSCIRC) and Departments of Center (KSCIRC) and Departments of Radial glia (RG) are primarily 2Neurological Surgery, 3Anatomical Sciences Radial glia (RG) are primarily 2Neurological Surgery, 3Anatomical Sciences Radial glia (RG) are primarily 2Neurological Surgery, 3Anatomical Sciences embryonic neuroglial progenitors that express and Neurobiology, University of Louisville embryonic neuroglial progenitors that express and Neurobiology, University of Louisville embryonic neuroglial progenitors that express and Neurobiology, University of Louisville Brain Lipid Binding Protein (Blbp a.k.a. Fabp7) School of Medicine, and the 4Summer Research Brain Lipid Binding Protein (Blbp a.k.a. Fabp7) School of Medicine, and the 4Summer Research Brain Lipid Binding Protein (Blbp a.k.a. Fabp7) School of Medicine, and the 4Summer Research and Glial Fibrillary Acidic Protein (Gfap). We Scholar’s Program, University of Louisville and Glial Fibrillary Acidic Protein (Gfap). We Scholar’s Program, University of Louisville and Glial Fibrillary Acidic Protein (Gfap). We Scholar’s Program, University of Louisville used these transcripts to demarcate the School of Medicine. used these transcripts to demarcate the School of Medicine. used these transcripts to demarcate the School of Medicine. distribution of spinal cord radial glia (SCRG) distribution of spinal cord radial glia (SCRG) distribution of spinal cord radial glia (SCRG) and screen for SCRG gene expression in the Spinal cord injury (SCI) results in and screen for SCRG gene expression in the Spinal cord injury (SCI) results in and screen for SCRG gene expression in the Spinal cord injury (SCI) results in Allen Spinal Cord Atlas (ASCA). We reveal immediate loss of microvascular Allen Spinal Cord Atlas (ASCA). We reveal immediate loss of microvascular Allen Spinal Cord Atlas (ASCA). We reveal immediate loss of microvascular that neonatal and adult SCRG are anchored in a function/structure at the injury site. A that neonatal and adult SCRG are anchored in a function/structure at the injury site. A that neonatal and adult SCRG are anchored in a function/structure at the injury site. A non-ventricular niche at the spinal cord (SC) temporally specific adaptive angiogenic non-ventricular niche at the spinal cord (SC) temporally specific adaptive angiogenic non-ventricular niche at the spinal cord (SC) temporally specific adaptive angiogenic pial boundary, and express a “signature” subset response occurs at the injury site over the first pial boundary, and express a “signature” subset response occurs at the injury site over the first pial boundary, and express a “signature” subset response occurs at the injury site over the first of 122 genes, many of which are shared with week post-SCI. These newly formed vessels of 122 genes, many of which are shared with week post-SCI. These newly formed vessels of 122 genes, many of which are shared with week post-SCI. These newly formed vessels “classic” neural stem cells (NSCs) of the exhibit abnormal structure and function, the “classic” neural stem cells (NSCs) of the exhibit abnormal structure and function, the “classic” neural stem cells (NSCs) of the exhibit abnormal structure and function, the subventricular zone (SVZ) and SC central canal effectors of which remain poorly understood. subventricular zone (SVZ) and SC central canal effectors of which remain poorly understood. subventricular zone (SVZ) and SC central canal effectors of which remain poorly understood. (CC). A core expressed gene set shared between Previous work demonstrated the up-regulation (CC). A core expressed gene set shared between Previous work demonstrated the up-regulation (CC). A core expressed gene set shared between Previous work demonstrated the up-regulation

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 67 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 67 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 67 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO of plasmalemmal vesicle associated protein P-54 Thrombin Inhbits Adult Neural of plasmalemmal vesicle associated protein P-54 Thrombin Inhbits Adult Neural of plasmalemmal vesicle associated protein P-54 Thrombin Inhbits Adult Neural (PV-1) expression in neovessels in/around the Progenitor Integration And Regeneration By (PV-1) expression in neovessels in/around the Progenitor Integration And Regeneration By (PV-1) expression in neovessels in/around the Progenitor Integration And Regeneration By injury site (Mozer et al., 2010). This is Promoting Astrogliogenesis Via Id1. injury site (Mozer et al., 2010). This is Promoting Astrogliogenesis Via Id1. injury site (Mozer et al., 2010). This is Promoting Astrogliogenesis Via Id1. significant as PV-1 is hallmark of fenestrated significant as PV-1 is hallmark of fenestrated significant as PV-1 is hallmark of fenestrated endothelia found in endocrine and pulmonary D. L. Sellers1,2, M. E. Gill1, D. O. Maris1,2, D. J. endothelia found in endocrine and pulmonary D. L. Sellers1,2, M. E. Gill1, D. O. Maris1,2, D. J. endothelia found in endocrine and pulmonary D. L. Sellers1,2, M. E. Gill1, D. O. Maris1,2, D. J. tissue, where free passage of molecules and Calkins4, P. J. Horner1,2,3 tissue, where free passage of molecules and Calkins4, P. J. Horner1,2,3 tissue, where free passage of molecules and Calkins4, P. J. Horner1,2,3 cells is desired. The goal of the current study 1 Department of Neurological Surgery, cells is desired. The goal of the current study 1 Department of Neurological Surgery, cells is desired. The goal of the current study 1 Department of Neurological Surgery, was to more precisely identify the University of Washington, Seattle, Washington, was to more precisely identify the University of Washington, Seattle, Washington, was to more precisely identify the University of Washington, Seattle, Washington, temporospatial appearance of these PV-1- 98104, USA; 2 Institute for Stem Cell and temporospatial appearance of these PV-1- 98104, USA; 2 Institute for Stem Cell and temporospatial appearance of these PV-1- 98104, USA; 2 Institute for Stem Cell and expressing microvessels and to better determine Regenerative Medicine, University of expressing microvessels and to better determine Regenerative Medicine, University of expressing microvessels and to better determine Regenerative Medicine, University of their functional state. Adult female C57bl/6 Washington, Seattle, Washington, 98195, USA; their functional state. Adult female C57bl/6 Washington, Seattle, Washington, 98195, USA; their functional state. Adult female C57bl/6 Washington, Seattle, Washington, 98195, USA; mice (n=18) received a moderately severe 3 Neurobiology and Behavior Program; Center mice (n=18) received a moderately severe 3 Neurobiology and Behavior Program; Center mice (n=18) received a moderately severe 3 Neurobiology and Behavior Program; Center contusive spinal cord injury. Mice were on Human Development and Disability; 4 The contusive spinal cord injury. Mice were on Human Development and Disability; 4 The contusive spinal cord injury. Mice were on Human Development and Disability; 4 The euthanized at 1,3, and 7 days post-SCI and Vanderbilt Eye Institute and Vanderbilt Brain euthanized at 1,3, and 7 days post-SCI and Vanderbilt Eye Institute and Vanderbilt Brain euthanized at 1,3, and 7 days post-SCI and Vanderbilt Eye Institute and Vanderbilt Brain spinal tissue was prepared for PV-1 Institute, Vanderbilt University School of spinal tissue was prepared for PV-1 Institute, Vanderbilt University School of spinal tissue was prepared for PV-1 Institute, Vanderbilt University School of immunohistochemistry. PV-1 expression Medicine, 11435 MRB IV, 2215B Garland immunohistochemistry. PV-1 expression Medicine, 11435 MRB IV, 2215B Garland immunohistochemistry. PV-1 expression Medicine, 11435 MRB IV, 2215B Garland patterns in serial sections representing one-half Avenue, Nashville, Tennessee, 37232. patterns in serial sections representing one-half Avenue, Nashville, Tennessee, 37232. patterns in serial sections representing one-half Avenue, Nashville, Tennessee, 37232. of the injury site (i.e. 500μm) were of the injury site (i.e. 500μm) were of the injury site (i.e. 500μm) were reconstructed 3-dimensionally. Qualitatively, The instructive cues that coordinate progenitor reconstructed 3-dimensionally. Qualitatively, The instructive cues that coordinate progenitor reconstructed 3-dimensionally. Qualitatively, The instructive cues that coordinate progenitor PV-1 expression peaks at 7 days SCI, consistent activation and fate specification early after PV-1 expression peaks at 7 days SCI, consistent activation and fate specification early after PV-1 expression peaks at 7 days SCI, consistent activation and fate specification early after with the previous study. Interestingly, in earlier injury remain largely unknown. Since thrombin with the previous study. Interestingly, in earlier injury remain largely unknown. Since thrombin with the previous study. Interestingly, in earlier injury remain largely unknown. Since thrombin time-points, PV-1 is initially seen in radicular sensing is a key stem cell trait, and blood time-points, PV-1 is initially seen in radicular sensing is a key stem cell trait, and blood time-points, PV-1 is initially seen in radicular sensing is a key stem cell trait, and blood vessels, eventually repopulating affected gray extravasation is a hallmark of trauma, we vessels, eventually repopulating affected gray extravasation is a hallmark of trauma, we vessels, eventually repopulating affected gray extravasation is a hallmark of trauma, we matter only and then later spreads diffusely examined the effects of thrombin on the matter only and then later spreads diffusely examined the effects of thrombin on the matter only and then later spreads diffusely examined the effects of thrombin on the throughout the epicenter. Importantly, PV-1 is proliferation and differentiation of adult neural throughout the epicenter. Importantly, PV-1 is proliferation and differentiation of adult neural throughout the epicenter. Importantly, PV-1 is proliferation and differentiation of adult neural restricted to microvessels devoid of astroglial progenitors (aNPC). Direct injection of restricted to microvessels devoid of astroglial progenitors (aNPC). Direct injection of restricted to microvessels devoid of astroglial progenitors (aNPC). Direct injection of investment and is absent in focal areas thrombin, in vivo, increased endogenous aNPC investment and is absent in focal areas thrombin, in vivo, increased endogenous aNPC investment and is absent in focal areas thrombin, in vivo, increased endogenous aNPC containing significant inflammatory infiltrate. proliferation 3-fold. Thrombin inhibition containing significant inflammatory infiltrate. proliferation 3-fold. Thrombin inhibition containing significant inflammatory infiltrate. proliferation 3-fold. Thrombin inhibition Further, caveolae formation appears to be reduced proliferation and astrogliogenesis after Further, caveolae formation appears to be reduced proliferation and astrogliogenesis after Further, caveolae formation appears to be reduced proliferation and astrogliogenesis after elevated in PV-1-expressing microvessels, spinal cord injury (SCI). Thrombin-treated elevated in PV-1-expressing microvessels, spinal cord injury (SCI). Thrombin-treated elevated in PV-1-expressing microvessels, spinal cord injury (SCI). Thrombin-treated suggesting increased trans-endothelial transport aNPC cultures increased proliferation versus suggesting increased trans-endothelial transport aNPC cultures increased proliferation versus suggesting increased trans-endothelial transport aNPC cultures increased proliferation versus potential. Lastly, using a novel model of in control cells, in vitro. Moreover, aNPCs became potential. Lastly, using a novel model of in control cells, in vitro. Moreover, aNPCs became potential. Lastly, using a novel model of in control cells, in vitro. Moreover, aNPCs became vitro CNS angiogenesis, PV-1 expression arises astrogliogenic when treated with thrombin and vitro CNS angiogenesis, PV-1 expression arises astrogliogenic when treated with thrombin and vitro CNS angiogenesis, PV-1 expression arises astrogliogenic when treated with thrombin and concomitant with vascular remodeling, continued to proliferate. Thrombin-treated cells concomitant with vascular remodeling, continued to proliferate. Thrombin-treated cells concomitant with vascular remodeling, continued to proliferate. Thrombin-treated cells suggesting that its expression is conserved up-regulated Inhibitors of DNA-binding (Id) suggesting that its expression is conserved up-regulated Inhibitors of DNA-binding (Id) suggesting that its expression is conserved up-regulated Inhibitors of DNA-binding (Id) during revascularization in various CNS areas. expression, which was demonstrated by shRNA during revascularization in various CNS areas. expression, which was demonstrated by shRNA during revascularization in various CNS areas. expression, which was demonstrated by shRNA These data are significant as they suggest that to promote astrocyte formation and inhibit These data are significant as they suggest that to promote astrocyte formation and inhibit These data are significant as they suggest that to promote astrocyte formation and inhibit angiogenesis post-SCI may be the consequence neuronal and oligodendroglial differentiation. angiogenesis post-SCI may be the consequence neuronal and oligodendroglial differentiation. angiogenesis post-SCI may be the consequence neuronal and oligodendroglial differentiation. of ingrowth by “non-parenchymal” vessels, When applied in vivo, transplanted aNPC of ingrowth by “non-parenchymal” vessels, When applied in vivo, transplanted aNPC of ingrowth by “non-parenchymal” vessels, When applied in vivo, transplanted aNPC explaining the consistent dysfunction in these integrated into the lesion, wrapped axons, and explaining the consistent dysfunction in these integrated into the lesion, wrapped axons, and explaining the consistent dysfunction in these integrated into the lesion, wrapped axons, and diffuse neo-vascular networks. regenerated myelin rings with thrombin diffuse neo-vascular networks. regenerated myelin rings with thrombin diffuse neo-vascular networks. regenerated myelin rings with thrombin This work was supported by a stipend provided inhibition. Together, these data demonstrate This work was supported by a stipend provided inhibition. Together, these data demonstrate This work was supported by a stipend provided inhibition. Together, these data demonstrate by the SRSP (APM) and a grant from the thrombin acts as a blood-borne early-response by the SRSP (APM) and a grant from the thrombin acts as a blood-borne early-response by the SRSP (APM) and a grant from the thrombin acts as a blood-borne early-response Kentucky Spinal Cord and Head Injury factor capable of directing differentiation and Kentucky Spinal Cord and Head Injury factor capable of directing differentiation and Kentucky Spinal Cord and Head Injury factor capable of directing differentiation and Research Trust (RLB). scar formation in the post-injury niche. This Research Trust (RLB). scar formation in the post-injury niche. This Research Trust (RLB). scar formation in the post-injury niche. This work supported by NIH, The Paralysis Project, work supported by NIH, The Paralysis Project, work supported by NIH, The Paralysis Project,

68 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 68 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 68 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

Paralyzed Veterans of America and The Neilsen recovery is only significantly improved in Paralyzed Veterans of America and The Neilsen recovery is only significantly improved in Paralyzed Veterans of America and The Neilsen recovery is only significantly improved in Foundation. animals subjected to cell transplantation alone Foundation. animals subjected to cell transplantation alone Foundation. animals subjected to cell transplantation alone or combined with decorin infusion, and there is or combined with decorin infusion, and there is or combined with decorin infusion, and there is P-55 Transplantation of Human Mpcs In prolonged survival of donor hMPCs after P-55 Transplantation of Human Mpcs In prolonged survival of donor hMPCs after P-55 Transplantation of Human Mpcs In prolonged survival of donor hMPCs after Combination With Scar Reducing Decorin decorin infusion for at least 2mo post SCI, Combination With Scar Reducing Decorin decorin infusion for at least 2mo post SCI, Combination With Scar Reducing Decorin decorin infusion for at least 2mo post SCI, Following Acute And Chronic Spinal Cord although numbers still decline over time. Following Acute And Chronic Spinal Cord although numbers still decline over time. Following Acute And Chronic Spinal Cord although numbers still decline over time. Injury In The Rat. Decorin treatment appears to moderately Injury In The Rat. Decorin treatment appears to moderately Injury In The Rat. Decorin treatment appears to moderately enhance tissue sparing. In addition, there are enhance tissue sparing. In addition, there are enhance tissue sparing. In addition, there are S.I. Hodgetts1, P.J. Simmons2, A. Buckley1, G.W. reduced numbers of infiltrating macrophages S.I. Hodgetts1, P.J. Simmons2, A. Buckley1, G.W. reduced numbers of infiltrating macrophages S.I. Hodgetts1, P.J. Simmons2, A. Buckley1, G.W. reduced numbers of infiltrating macrophages Plant1,3 with either core/non-core decorin isoforms. Plant1,3 with either core/non-core decorin isoforms. Plant1,3 with either core/non-core decorin isoforms. Red’s Spinal Cord Research Neuronal expression profiles of proteins (RT97, Red’s Spinal Cord Research Neuronal expression profiles of proteins (RT97, Red’s Spinal Cord Research Neuronal expression profiles of proteins (RT97, Laboratory1, School of Anatomy and Human GFAP, BetaIIITubulin and CGRP) are apparent Laboratory1, School of Anatomy and Human GFAP, BetaIIITubulin and CGRP) are apparent Laboratory1, School of Anatomy and Human GFAP, BetaIIITubulin and CGRP) are apparent Biology, University of Western Australia, Perth, centrally within the lesion sites of many hMPC- Biology, University of Western Australia, Perth, centrally within the lesion sites of many hMPC- Biology, University of Western Australia, Perth, centrally within the lesion sites of many hMPC- Australia; Brown Foundation Institute of treated, hMPC/decorin infusion-treated and Australia; Brown Foundation Institute of treated, hMPC/decorin infusion-treated and Australia; Brown Foundation Institute of treated, hMPC/decorin infusion-treated and Molecular Medicine, University of Texas Health even decorin only-infused (either isoform) Molecular Medicine, University of Texas Health even decorin only-infused (either isoform) Molecular Medicine, University of Texas Health even decorin only-infused (either isoform) Science Center 2, Houston, USA; Stanford animals. ECM expression and molecules Science Center 2, Houston, USA; Stanford animals. ECM expression and molecules Science Center 2, Houston, USA; Stanford animals. ECM expression and molecules Partnership for Spinal Cord Injury and Repair, associated with glial scar tissue (Collagen, Partnership for Spinal Cord Injury and Repair, associated with glial scar tissue (Collagen, Partnership for Spinal Cord Injury and Repair, associated with glial scar tissue (Collagen, Department of Neurosurgery, Stanford neurocan, phosphocan) in decorin infused Department of Neurosurgery, Stanford neurocan, phosphocan) in decorin infused Department of Neurosurgery, Stanford neurocan, phosphocan) in decorin infused University School of Medicine,3 Stanford animals trends toward being slightly reduced University School of Medicine,3 Stanford animals trends toward being slightly reduced University School of Medicine,3 Stanford animals trends toward being slightly reduced University, Stanford, USA compared to donor hMPC-treatment (alone). University, Stanford, USA compared to donor hMPC-treatment (alone). University, Stanford, USA compared to donor hMPC-treatment (alone). Decorin may be incorporated into combinatorial Decorin may be incorporated into combinatorial Decorin may be incorporated into combinatorial Human mesenchymal precursor cells treatments to promote improved donor cell Human mesenchymal precursor cells treatments to promote improved donor cell Human mesenchymal precursor cells treatments to promote improved donor cell (hMPCs) isolated from bone marrow stroma of survival and reduced secondary damage after (hMPCs) isolated from bone marrow stroma of survival and reduced secondary damage after (hMPCs) isolated from bone marrow stroma of survival and reduced secondary damage after spinal cord injured patients were transplanted acute/chronic SCI. spinal cord injured patients were transplanted acute/chronic SCI. spinal cord injured patients were transplanted acute/chronic SCI. into the spinal cord of Nude (immunodeficient) into the spinal cord of Nude (immunodeficient) into the spinal cord of Nude (immunodeficient) rats both alone and in combination with the scar P-56 Self-renewal and multipotential rats both alone and in combination with the scar P-56 Self-renewal and multipotential rats both alone and in combination with the scar P-56 Self-renewal and multipotential reducing compound decorin after acute properties of GFAP-expressing cell reducing compound decorin after acute properties of GFAP-expressing cell reducing compound decorin after acute properties of GFAP-expressing cell (immediate) and chronic (long term) spinal cord populations in the adult spinal cord (immediate) and chronic (long term) spinal cord populations in the adult spinal cord (immediate) and chronic (long term) spinal cord populations in the adult spinal cord injury (SCI). Functional recovery after highly injury (SCI). Functional recovery after highly injury (SCI). Functional recovery after highly purified human decorin infusion (core and non- R. Fiorelli & O. Raineteau purified human decorin infusion (core and non- R. Fiorelli & O. Raineteau purified human decorin infusion (core and non- R. Fiorelli & O. Raineteau core isoforms) via minipump was assessed using Brain Research Institute, University of core isoforms) via minipump was assessed using Brain Research Institute, University of core isoforms) via minipump was assessed using Brain Research Institute, University of open field (BBB) and Catwalk gait analysis for Zurich/ETHZ, Switzerland open field (BBB) and Catwalk gait analysis for Zurich/ETHZ, Switzerland open field (BBB) and Catwalk gait analysis for Zurich/ETHZ, Switzerland up to 3mo post SCI. Morphological analysis of up to 3mo post SCI. Morphological analysis of up to 3mo post SCI. Morphological analysis of neuronal marker expression profiles, cyst size, Neural Stem Cells (NSCs) cells can be neuronal marker expression profiles, cyst size, Neural Stem Cells (NSCs) cells can be neuronal marker expression profiles, cyst size, Neural Stem Cells (NSCs) cells can be tissue sparing, macrophage infiltration and found throughout the adult central nervous tissue sparing, macrophage infiltration and found throughout the adult central nervous tissue sparing, macrophage infiltration and found throughout the adult central nervous extracellular matrix (ECM) deposition/glial system (CNS), although neurogenesis is extracellular matrix (ECM) deposition/glial system (CNS), although neurogenesis is extracellular matrix (ECM) deposition/glial system (CNS), although neurogenesis is scarring in and around the injury site was also restricted to a few regions. In the forebrain sub- scarring in and around the injury site was also restricted to a few regions. In the forebrain sub- scarring in and around the injury site was also restricted to a few regions. In the forebrain sub- assessed. Extensive analysis of hMPCs axonal ependymal zone (SEZ), neurons originate from assessed. Extensive analysis of hMPCs axonal ependymal zone (SEZ), neurons originate from assessed. Extensive analysis of hMPCs axonal ependymal zone (SEZ), neurons originate from growth stimulating potential in vitro using co- NSCs expressing the astrocytic marker GFAP. growth stimulating potential in vitro using co- NSCs expressing the astrocytic marker GFAP. growth stimulating potential in vitro using co- NSCs expressing the astrocytic marker GFAP. cultures of hMPCs with embryonic DRG In other regions of the adult CNS such as the cultures of hMPCs with embryonic DRG In other regions of the adult CNS such as the cultures of hMPCs with embryonic DRG In other regions of the adult CNS such as the explants revealed that neurite growth is spinal cord, cells showing NSCs properties can explants revealed that neurite growth is spinal cord, cells showing NSCs properties can explants revealed that neurite growth is spinal cord, cells showing NSCs properties can markedly improved with hMPC co-culture but is be isolated in vitro, but their identity remains markedly improved with hMPC co-culture but is be isolated in vitro, but their identity remains markedly improved with hMPC co-culture but is be isolated in vitro, but their identity remains not further enhanced in combination with either elusive. Here, we used a transgenic inducible not further enhanced in combination with either elusive. Here, we used a transgenic inducible not further enhanced in combination with either elusive. Here, we used a transgenic inducible decorin isoform and there is no growth mouse (hGFAP-CreERT2 x Stop-RosaYFP) to decorin isoform and there is no growth mouse (hGFAP-CreERT2 x Stop-RosaYFP) to decorin isoform and there is no growth mouse (hGFAP-CreERT2 x Stop-RosaYFP) to promotion of either decorin isoform with DRG label and fate map putative GFAP(+) NSCs promotion of either decorin isoform with DRG label and fate map putative GFAP(+) NSCs promotion of either decorin isoform with DRG label and fate map putative GFAP(+) NSCs alone. In acute and chronic SCI: functional populations in the adult SEZ and spinal cord alone. In acute and chronic SCI: functional populations in the adult SEZ and spinal cord alone. In acute and chronic SCI: functional populations in the adult SEZ and spinal cord

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 69 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 69 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 69 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

(SC), and compare their self-renewal and following neurological injury. However, (SC), and compare their self-renewal and following neurological injury. However, (SC), and compare their self-renewal and following neurological injury. However, multipotential properties. Recombined SEZ previous works focus on improvements multipotential properties. Recombined SEZ previous works focus on improvements multipotential properties. Recombined SEZ previous works focus on improvements NSCs could be identified based on their markers observed within the training devices, when NSCs could be identified based on their markers observed within the training devices, when NSCs could be identified based on their markers observed within the training devices, when expression (i.e. Vimentin, Nestin), proliferative improvements found in more normal, everyday expression (i.e. Vimentin, Nestin), proliferative improvements found in more normal, everyday expression (i.e. Vimentin, Nestin), proliferative improvements found in more normal, everyday properties, and by their capacity to continuously activities should be the main goal. To address properties, and by their capacity to continuously activities should be the main goal. To address properties, and by their capacity to continuously activities should be the main goal. To address give rise to olfactory neurons. In the SC, this, we train rats following a right cervical give rise to olfactory neurons. In the SC, this, we train rats following a right cervical give rise to olfactory neurons. In the SC, this, we train rats following a right cervical recombination occurred in the vast majority of overhemisection injury with a robotic gait recombination occurred in the vast majority of overhemisection injury with a robotic gait recombination occurred in the vast majority of overhemisection injury with a robotic gait parenchymal astrocytes as well as in a minor trainer (RRMPS, Robomedica Inc, Irvine CA) parenchymal astrocytes as well as in a minor trainer (RRMPS, Robomedica Inc, Irvine CA) parenchymal astrocytes as well as in a minor trainer (RRMPS, Robomedica Inc, Irvine CA) population of sub-ependymal, bipolar GFAP+ but assess recovery of overground locomotion population of sub-ependymal, bipolar GFAP+ but assess recovery of overground locomotion population of sub-ependymal, bipolar GFAP+ but assess recovery of overground locomotion cells surrounding the central canal (CC). These with the CatWalk gait analysis system (Noldus, cells surrounding the central canal (CC). These with the CatWalk gait analysis system (Noldus, cells surrounding the central canal (CC). These with the CatWalk gait analysis system (Noldus, cells expressed similar markers to SEZ-NSCs, Wageningen, NE). Many measures of cells expressed similar markers to SEZ-NSCs, Wageningen, NE). Many measures of cells expressed similar markers to SEZ-NSCs, Wageningen, NE). Many measures of while parenchyma GFAP+ astrocytes acquired overground locomotion are dependent on while parenchyma GFAP+ astrocytes acquired overground locomotion are dependent on while parenchyma GFAP+ astrocytes acquired overground locomotion are dependent on these markers (i.e. Vimentin, Nestin) after walking velocity (short strides are taken these markers (i.e. Vimentin, Nestin) after walking velocity (short strides are taken these markers (i.e. Vimentin, Nestin) after walking velocity (short strides are taken injury. We next assessed the NSCs properties of gradually when walking slow; long strides are injury. We next assessed the NSCs properties of gradually when walking slow; long strides are injury. We next assessed the NSCs properties of gradually when walking slow; long strides are these two cell populations in an in vitro taken rapidly when walking fast). Therefore, these two cell populations in an in vitro taken rapidly when walking fast). Therefore, these two cell populations in an in vitro taken rapidly when walking fast). Therefore, neurosphere assay. Primary neurospheres were we have developed a nonlinear regression neurosphere assay. Primary neurospheres were we have developed a nonlinear regression neurosphere assay. Primary neurospheres were we have developed a nonlinear regression successfully obtained from both the intact and analysis technique to parse out which changes in successfully obtained from both the intact and analysis technique to parse out which changes in successfully obtained from both the intact and analysis technique to parse out which changes in injured spinal cord, and in both conditions, overground locomotion are due to neurological injured spinal cord, and in both conditions, overground locomotion are due to neurological injured spinal cord, and in both conditions, overground locomotion are due to neurological ~20% of the spheres expressed the YFP reporter impairments and not simply a difference in ~20% of the spheres expressed the YFP reporter impairments and not simply a difference in ~20% of the spheres expressed the YFP reporter impairments and not simply a difference in gene indicating their origin from GFAP walking speed. Several styles of robotic gait gene indicating their origin from GFAP walking speed. Several styles of robotic gait gene indicating their origin from GFAP walking speed. Several styles of robotic gait expressing cells. These neurospheres were training were applied daily over a four week expressing cells. These neurospheres were training were applied daily over a four week expressing cells. These neurospheres were training were applied daily over a four week shown to be multipotent. Noticeably, while period. As is often done in the clinical setting, shown to be multipotent. Noticeably, while period. As is often done in the clinical setting, shown to be multipotent. Noticeably, while period. As is often done in the clinical setting, YFP+ neurospheres derived from intact SC we applied the average pre-injury stepping YFP+ neurospheres derived from intact SC we applied the average pre-injury stepping YFP+ neurospheres derived from intact SC we applied the average pre-injury stepping could not be passaged for extended periods of patterns to one group of injured animals. This could not be passaged for extended periods of patterns to one group of injured animals. This could not be passaged for extended periods of patterns to one group of injured animals. This time, those from the injury showed prolonged practice depends on precise alignment and time, those from the injury showed prolonged practice depends on precise alignment and time, those from the injury showed prolonged practice depends on precise alignment and self-renewal properties. All together, our work timing to match the guiding forces with the self-renewal properties. All together, our work timing to match the guiding forces with the self-renewal properties. All together, our work timing to match the guiding forces with the reveals major differences in the identity of stem animals walking. In contrast, training was also reveals major differences in the identity of stem animals walking. In contrast, training was also reveals major differences in the identity of stem animals walking. In contrast, training was also and progenitor cells in distinct regions of the performed in viscous and negative viscosity and progenitor cells in distinct regions of the performed in viscous and negative viscosity and progenitor cells in distinct regions of the performed in viscous and negative viscosity adult CNS; our results further suggest that fields. An untrained group, and a daily training adult CNS; our results further suggest that fields. An untrained group, and a daily training adult CNS; our results further suggest that fields. An untrained group, and a daily training parenchyma reactive astrocytes may represent a without robotic forces (null field) group were parenchyma reactive astrocytes may represent a without robotic forces (null field) group were parenchyma reactive astrocytes may represent a without robotic forces (null field) group were minor population of NSCs that are recruited used as controls. After four weeks of training, minor population of NSCs that are recruited used as controls. After four weeks of training, minor population of NSCs that are recruited used as controls. After four weeks of training, after spinal cord injury. the pre-injury pattern and null field groups both after spinal cord injury. the pre-injury pattern and null field groups both after spinal cord injury. the pre-injury pattern and null field groups both exhibited less overground locomotor deficits exhibited less overground locomotor deficits exhibited less overground locomotor deficits P-57 Optimizing Recovery Of Overground than the untrained group. However, two weeks P-57 Optimizing Recovery Of Overground than the untrained group. However, two weeks P-57 Optimizing Recovery Of Overground than the untrained group. However, two weeks Locomotion With Novel Robotic Gait after the cessation of training the pre-injury Locomotion With Novel Robotic Gait after the cessation of training the pre-injury Locomotion With Novel Robotic Gait after the cessation of training the pre-injury Training Patterns Following SCI In Rats pattern group maintained their improvements, Training Patterns Following SCI In Rats pattern group maintained their improvements, Training Patterns Following SCI In Rats pattern group maintained their improvements, while the null field did not. Results from the while the null field did not. Results from the while the null field did not. Results from the ND Neckel1, H. Dai1, J. Laracy1, M. McAtee1, C. viscous and negative viscosity trained groups ND Neckel1, H. Dai1, J. Laracy1, M. McAtee1, C. viscous and negative viscosity trained groups ND Neckel1, H. Dai1, J. Laracy1, M. McAtee1, C. viscous and negative viscosity trained groups Soper1, B. Bregman1 are promising, but statistically inconclusive at Soper1, B. Bregman1 are promising, but statistically inconclusive at Soper1, B. Bregman1 are promising, but statistically inconclusive at 1Georgetown University, Dept. of this time. 1Georgetown University, Dept. of this time. 1Georgetown University, Dept. of this time. Neuroscience, Washington DC, USA Neuroscience, Washington DC, USA Neuroscience, Washington DC, USA P-58 Robotic Training In Spinal Rats P-58 Robotic Training In Spinal Rats P-58 Robotic Training In Spinal Rats In both clinical and experimental Produces Novel Gait Patterns And In both clinical and experimental Produces Novel Gait Patterns And In both clinical and experimental Produces Novel Gait Patterns And settings, robotic gait training has become a Abnormally High Levels Of Glutamate And settings, robotic gait training has become a Abnormally High Levels Of Glutamate And settings, robotic gait training has become a Abnormally High Levels Of Glutamate And popular means to encourage neuronal plasticity Glycine In The Lumbar Spinal Cord popular means to encourage neuronal plasticity Glycine In The Lumbar Spinal Cord popular means to encourage neuronal plasticity Glycine In The Lumbar Spinal Cord in an effort to facilitate functional recovery in an effort to facilitate functional recovery in an effort to facilitate functional recovery

70 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 70 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 70 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

P.A. See, E. Partida, M.J. Cantoria, H. Singh, V.S. Boyce1, J. Park1, F.H. Gage2 and L.M. P.A. See, E. Partida, M.J. Cantoria, H. Singh, V.S. Boyce1, J. Park1, F.H. Gage2 and L.M. P.A. See, E. Partida, M.J. Cantoria, H. Singh, V.S. Boyce1, J. Park1, F.H. Gage2 and L.M. R.D. de Leon Mendell1 R.D. de Leon Mendell1 R.D. de Leon Mendell1 California State University - Los 1 Department of Neurobiology and California State University - Los 1 Department of Neurobiology and California State University - Los 1 Department of Neurobiology and Angeles, School of Kinesiology and Nutritional Behavior, State University of New York at Stony Angeles, School of Kinesiology and Nutritional Behavior, State University of New York at Stony Angeles, School of Kinesiology and Nutritional Behavior, State University of New York at Stony Science, 5151 State University Drive, Los Brook, Stony Brook NY; 2 Laboratory of Science, 5151 State University Drive, Los Brook, Stony Brook NY; 2 Laboratory of Science, 5151 State University Drive, Los Brook, Stony Brook NY; 2 Laboratory of Angeles, CA USA Genetics, Salk Institute, La Jolla, CA Angeles, CA USA Genetics, Salk Institute, La Jolla, CA Angeles, CA USA Genetics, Salk Institute, La Jolla, CA

After spinal cord transection, the We sought to determine an effective After spinal cord transection, the We sought to determine an effective After spinal cord transection, the We sought to determine an effective generation of stepping depends on dose of BDNF necessary to promote the generation of stepping depends on dose of BDNF necessary to promote the generation of stepping depends on dose of BDNF necessary to promote the neurotransmitter systems entirely contained recovery of stepping in adult spinal rats. neurotransmitter systems entirely contained recovery of stepping in adult spinal rats. neurotransmitter systems entirely contained recovery of stepping in adult spinal rats. within the local lumbar spinal cord. Glutamate Following a complete T10 spinal cord within the local lumbar spinal cord. Glutamate Following a complete T10 spinal cord within the local lumbar spinal cord. Glutamate Following a complete T10 spinal cord and glycine likely play important roles, but transection injury, adult rats were immediately and glycine likely play important roles, but transection injury, adult rats were immediately and glycine likely play important roles, but transection injury, adult rats were immediately surprisingly, little is known about how the treated with BDNF delivered to the lesion via surprisingly, little is known about how the treated with BDNF delivered to the lesion via surprisingly, little is known about how the treated with BDNF delivered to the lesion via content of these two key neurotransmitters intraspinal injections of adeno associated viral content of these two key neurotransmitters intraspinal injections of adeno associated viral content of these two key neurotransmitters intraspinal injections of adeno associated viral changes in order to achieve weight bearing (AAV) constructs. Three different viral titers changes in order to achieve weight bearing (AAV) constructs. Three different viral titers changes in order to achieve weight bearing (AAV) constructs. Three different viral titers stepping after spinal cord injury. We studied the were used, low (5x109 genomic copies (gc)), stepping after spinal cord injury. We studied the were used, low (5x109 genomic copies (gc)), stepping after spinal cord injury. We studied the were used, low (5x109 genomic copies (gc)), levels of glutamate and glycine in the lumbar intermediate (1x1010) and high (2.5x1010). levels of glutamate and glycine in the lumbar intermediate (1x1010) and high (2.5x1010). levels of glutamate and glycine in the lumbar intermediate (1x1010) and high (2.5x1010). spinal cord of spinally transected rats. Rats Kinematic analysis of hindlimb locomotor spinal cord of spinally transected rats. Rats Kinematic analysis of hindlimb locomotor spinal cord of spinally transected rats. Rats Kinematic analysis of hindlimb locomotor (n=48) received spinal cord transection at five function revealed that animals receiving the (n=48) received spinal cord transection at five function revealed that animals receiving the (n=48) received spinal cord transection at five function revealed that animals receiving the days of age and four weeks later, half were highest dose recovered treadmill and over- days of age and four weeks later, half were highest dose recovered treadmill and over- days of age and four weeks later, half were highest dose recovered treadmill and over- trained to step using a robotic treadmill system ground stepping. Animals treated with low trained to step using a robotic treadmill system ground stepping. Animals treated with low trained to step using a robotic treadmill system ground stepping. Animals treated with low and the remaining half were untrained controls. AAV-BDNF could not step over-ground and and the remaining half were untrained controls. AAV-BDNF could not step over-ground and and the remaining half were untrained controls. AAV-BDNF could not step over-ground and Analyses of glutamate and glycine content via required perineal stimulation for treadmill Analyses of glutamate and glycine content via required perineal stimulation for treadmill Analyses of glutamate and glycine content via required perineal stimulation for treadmill high-performance liquid chromatography locomotion. Some rats receiving intermediate high-performance liquid chromatography locomotion. Some rats receiving intermediate high-performance liquid chromatography locomotion. Some rats receiving intermediate (HPLC) showed training significantly raised the AAV-BDNF recovered the capacity for both (HPLC) showed training significantly raised the AAV-BDNF recovered the capacity for both (HPLC) showed training significantly raised the AAV-BDNF recovered the capacity for both levels of both neurotransmitters in the lumbar over-ground and treadmill stepping. Plantar levels of both neurotransmitters in the lumbar over-ground and treadmill stepping. Plantar levels of both neurotransmitters in the lumbar over-ground and treadmill stepping. Plantar spinal cord beyond normal. In the Trained rats, testing demonstrated that reduced thermal spinal cord beyond normal. In the Trained rats, testing demonstrated that reduced thermal spinal cord beyond normal. In the Trained rats, testing demonstrated that reduced thermal glutamate and glycine levels were significantly withdrawal latency, indicative of enhanced glutamate and glycine levels were significantly withdrawal latency, indicative of enhanced glutamate and glycine levels were significantly withdrawal latency, indicative of enhanced correlated with the ability to perform responsiveness to noxious heat, developed in all correlated with the ability to perform responsiveness to noxious heat, developed in all correlated with the ability to perform responsiveness to noxious heat, developed in all independent stepping. Immunohistochemical BDNF treated rats. Hindlimb spasticity was also independent stepping. Immunohistochemical BDNF treated rats. Hindlimb spasticity was also independent stepping. Immunohistochemical BDNF treated rats. Hindlimb spasticity was also analyses showed that the expression of VGluT1 observed in rats in the high treatment group. In analyses showed that the expression of VGluT1 observed in rats in the high treatment group. In analyses showed that the expression of VGluT1 observed in rats in the high treatment group. In and GlyT2 around motor neurons was terminal electrophysiological experiments and GlyT2 around motor neurons was terminal electrophysiological experiments and GlyT2 around motor neurons was terminal electrophysiological experiments significantly greater in Trained versus Untrained rheobase (Rh) was determined in medial significantly greater in Trained versus Untrained rheobase (Rh) was determined in medial significantly greater in Trained versus Untrained rheobase (Rh) was determined in medial rats. Training improved the ability to generate gastrocnemius (MG) and lateral gastrocnemius rats. Training improved the ability to generate gastrocnemius (MG) and lateral gastrocnemius rats. Training improved the ability to generate gastrocnemius (MG) and lateral gastrocnemius stepping at a range of weight support levels, but soleus (LGS) motoneurons. Motoneurons of rats stepping at a range of weight support levels, but soleus (LGS) motoneurons. Motoneurons of rats stepping at a range of weight support levels, but soleus (LGS) motoneurons. Motoneurons of rats normal stepping characteristics were not receiving high BDNF titers were considerably normal stepping characteristics were not receiving high BDNF titers were considerably normal stepping characteristics were not receiving high BDNF titers were considerably restored by training. These findings suggested more excitable (Mean Rh: 5.4 ± 1.8 nA) than restored by training. These findings suggested more excitable (Mean Rh: 5.4 ± 1.8 nA) than restored by training. These findings suggested more excitable (Mean Rh: 5.4 ± 1.8 nA) than that training-induced adaptations in glutamate motoneurons in intermediate (Mean .Rh:7.2 ± that training-induced adaptations in glutamate motoneurons in intermediate (Mean .Rh:7.2 ± that training-induced adaptations in glutamate motoneurons in intermediate (Mean .Rh:7.2 ± and glycine levels played a role in the 3.5 nA) or low (Mean Rh: 9.4 ± 4.8nA) and glycine levels played a role in the 3.5 nA) or low (Mean Rh: 9.4 ± 4.8nA) and glycine levels played a role in the 3.5 nA) or low (Mean Rh: 9.4 ± 4.8nA) generation of novel gait patterns following treatment groups. In addition, c-Fos expression generation of novel gait patterns following treatment groups. In addition, c-Fos expression generation of novel gait patterns following treatment groups. In addition, c-Fos expression complete spinal cord transection. was significantly elevated in lamina VI-VII of complete spinal cord transection. was significantly elevated in lamina VI-VII of complete spinal cord transection. was significantly elevated in lamina VI-VII of the L2 spinal cord of rats in the high treatment the L2 spinal cord of rats in the high treatment the L2 spinal cord of rats in the high treatment P-59 Dose Dependant Effects of BDNF on group suggesting activation of central pattern P-59 Dose Dependant Effects of BDNF on group suggesting activation of central pattern P-59 Dose Dependant Effects of BDNF on group suggesting activation of central pattern Locomotor Recovery In Paraplegic Rats generator neurons with AAV-BDNF treatment. Locomotor Recovery In Paraplegic Rats generator neurons with AAV-BDNF treatment. Locomotor Recovery In Paraplegic Rats generator neurons with AAV-BDNF treatment. These results indicate that intermediate doses of These results indicate that intermediate doses of These results indicate that intermediate doses of AAV-BDNF may be sufficient for the recovery AAV-BDNF may be sufficient for the recovery AAV-BDNF may be sufficient for the recovery

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 71 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 71 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 71 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO of over-ground locomotion while reducing some administered by intraperitoneal injection at 30 of over-ground locomotion while reducing some administered by intraperitoneal injection at 30 of over-ground locomotion while reducing some administered by intraperitoneal injection at 30 of the adverse side effects (spasticity) observed minutes post-injury and then once per day for 7 of the adverse side effects (spasticity) observed minutes post-injury and then once per day for 7 of the adverse side effects (spasticity) observed minutes post-injury and then once per day for 7 at the highest dose. At present, it is not clear days. Hind limb locomotion was evaluated at the highest dose. At present, it is not clear days. Hind limb locomotion was evaluated at the highest dose. At present, it is not clear days. Hind limb locomotion was evaluated whether sensitization of nociceptive projections using the Basso, Beattie, Bresnahan (BBB) scale whether sensitization of nociceptive projections using the Basso, Beattie, Bresnahan (BBB) scale whether sensitization of nociceptive projections using the Basso, Beattie, Bresnahan (BBB) scale is necessary for the recovery of stepping, or and the Catwalk kinematic analysis once per is necessary for the recovery of stepping, or and the Catwalk kinematic analysis once per is necessary for the recovery of stepping, or and the Catwalk kinematic analysis once per whether this is unrelated and an adverse side week for 4 weeks post-SCI. At the conclusion of whether this is unrelated and an adverse side week for 4 weeks post-SCI. At the conclusion of whether this is unrelated and an adverse side week for 4 weeks post-SCI. At the conclusion of effect of BDNF treatment due to the generalized the behavioral evaluation, the spinal cord tissue effect of BDNF treatment due to the generalized the behavioral evaluation, the spinal cord tissue effect of BDNF treatment due to the generalized the behavioral evaluation, the spinal cord tissue hyperexcitability. was extracted and processed to evaluate hyperexcitability. was extracted and processed to evaluate hyperexcitability. was extracted and processed to evaluate numbers of ventral horn neurons and white numbers of ventral horn neurons and white numbers of ventral horn neurons and white P-60 Post-Injury Administration of An matter sparing. MnTE-2-PyP-treated rats had P-60 Post-Injury Administration of An matter sparing. MnTE-2-PyP-treated rats had P-60 Post-Injury Administration of An matter sparing. MnTE-2-PyP-treated rats had Oxidoreductant Confers Protection After significantly higher BBB scores and a greater Oxidoreductant Confers Protection After significantly higher BBB scores and a greater Oxidoreductant Confers Protection After significantly higher BBB scores and a greater Contusional Spinal Cord Injury In Adult average regularity index as compared to the Contusional Spinal Cord Injury In Adult average regularity index as compared to the Contusional Spinal Cord Injury In Adult average regularity index as compared to the Rats vehicle group. Preliminary analysis of the Rats vehicle group. Preliminary analysis of the Rats vehicle group. Preliminary analysis of the histological markers indicates an increase in histological markers indicates an increase in histological markers indicates an increase in K. Savage1, M. Girard1, H. M. Tse2, C. L. Floyd1 neuronal number and increase in white matter K. Savage1, M. Girard1, H. M. Tse2, C. L. Floyd1 neuronal number and increase in white matter K. Savage1, M. Girard1, H. M. Tse2, C. L. Floyd1 neuronal number and increase in white matter 1Departments of Physical Medicine and sparing in animals that received MnTE-2-PyP. 1Departments of Physical Medicine and sparing in animals that received MnTE-2-PyP. 1Departments of Physical Medicine and sparing in animals that received MnTE-2-PyP. Rehabilitation and 2Microbiology, University of These data suggest that post-SCI administration Rehabilitation and 2Microbiology, University of These data suggest that post-SCI administration Rehabilitation and 2Microbiology, University of These data suggest that post-SCI administration Alabama at Birmingham. Birmingham, of this novel oxidoreductant is protective in SCI Alabama at Birmingham. Birmingham, of this novel oxidoreductant is protective in SCI Alabama at Birmingham. Birmingham, of this novel oxidoreductant is protective in SCI Alabama, USA. and is a promising candidate for future Alabama, USA. and is a promising candidate for future Alabama, USA. and is a promising candidate for future The deleterious effects of oxidative development as a therapeutic. The deleterious effects of oxidative development as a therapeutic. The deleterious effects of oxidative development as a therapeutic. stress in spinal cord injury (SCI) have been stress in spinal cord injury (SCI) have been stress in spinal cord injury (SCI) have been previously described and detoxification of P-61 Fibronectin Administration Inhibits previously described and detoxification of P-61 Fibronectin Administration Inhibits previously described and detoxification of P-61 Fibronectin Administration Inhibits reactive oxygen species (ROS) is a well- Chronic Pain Development After Spinal reactive oxygen species (ROS) is a well- Chronic Pain Development After Spinal reactive oxygen species (ROS) is a well- Chronic Pain Development After Spinal documented therapeutic target for conferring Cord Injury documented therapeutic target for conferring Cord Injury documented therapeutic target for conferring Cord Injury cellular protection. Efforts to develop highly cellular protection. Efforts to develop highly cellular protection. Efforts to develop highly efficacious pharmacological agents to reduce C.-Y. Lin1, Y.-S. Lee2*, V. W. Lin3, J. Silver4 efficacious pharmacological agents to reduce C.-Y. Lin1, Y.-S. Lee2*, V. W. Lin3, J. Silver4 efficacious pharmacological agents to reduce C.-Y. Lin1, Y.-S. Lee2*, V. W. Lin3, J. Silver4 ROS have focused on the native defensive 1, 2 Department of Neurosciences, Lerner ROS have focused on the native defensive 1, 2 Department of Neurosciences, Lerner ROS have focused on the native defensive 1, 2 Department of Neurosciences, Lerner enzyme superoxide dismutase (SOD). Previous Research Institute, Cleveland Clinic, Cleveland, enzyme superoxide dismutase (SOD). Previous Research Institute, Cleveland Clinic, Cleveland, enzyme superoxide dismutase (SOD). Previous Research Institute, Cleveland Clinic, Cleveland, generation SOD compounds were poorly OH, USA, and 3Department of Physical generation SOD compounds were poorly OH, USA, and 3Department of Physical generation SOD compounds were poorly OH, USA, and 3Department of Physical translated to clinical use based on their large Medicine and Rehabilitation Cleveland Clinic, translated to clinical use based on their large Medicine and Rehabilitation Cleveland Clinic, translated to clinical use based on their large Medicine and Rehabilitation Cleveland Clinic, size, minimal cell permeability, short circulating Cleveland, OH, USA, and 4Department of size, minimal cell permeability, short circulating Cleveland, OH, USA, and 4Department of size, minimal cell permeability, short circulating Cleveland, OH, USA, and 4Department of half-life, and low bioavailability in target Neurosciences, Case Western Reserve half-life, and low bioavailability in target Neurosciences, Case Western Reserve half-life, and low bioavailability in target Neurosciences, Case Western Reserve tissues. Recently, a class of smaller SOD- University, Cleveland, OH, USA. tissues. Recently, a class of smaller SOD- University, Cleveland, OH, USA. tissues. Recently, a class of smaller SOD- University, Cleveland, OH, USA. mimetics have been developed which includes a mimetics have been developed which includes a mimetics have been developed which includes a very potent metalloporphyrin catalytic Chronic pain following spinal cord very potent metalloporphyrin catalytic Chronic pain following spinal cord very potent metalloporphyrin catalytic Chronic pain following spinal cord oxidoreductant, manganese (III)-tetrakis (N- injury (SCI) is a highly prevalent clinical oxidoreductant, manganese (III)-tetrakis (N- injury (SCI) is a highly prevalent clinical oxidoreductant, manganese (III)-tetrakis (N- injury (SCI) is a highly prevalent clinical ethylpyridinium-2-yl)porphyrin (MnTE-2-PyP), condition that is difficult to treat. Using both ethylpyridinium-2-yl)porphyrin (MnTE-2-PyP), condition that is difficult to treat. Using both ethylpyridinium-2-yl)porphyrin (MnTE-2-PyP), condition that is difficult to treat. Using both that is efficacious in scavenging a broad range von Frey filaments and radiant infrared heat to that is efficacious in scavenging a broad range von Frey filaments and radiant infrared heat to that is efficacious in scavenging a broad range von Frey filaments and radiant infrared heat to of ROS including superoxide, hydrogen assess mechanical allodynia and thermal of ROS including superoxide, hydrogen assess mechanical allodynia and thermal of ROS including superoxide, hydrogen assess mechanical allodynia and thermal peroxide, and peroxynitrite. In this study we hyperalgesia, respectively, we have peroxide, and peroxynitrite. In this study we hyperalgesia, respectively, we have peroxide, and peroxynitrite. In this study we hyperalgesia, respectively, we have evaluated the effect of post-SCI administration demonstrated that a one-time intraspinal injection evaluated the effect of post-SCI administration demonstrated that a one-time intraspinal injection evaluated the effect of post-SCI administration demonstrated that a one-time intraspinal injection of MnTE-2-PyP on tissue sparing and functional of fibronectin delivered acutely robustly inhibits the of MnTE-2-PyP on tissue sparing and functional of fibronectin delivered acutely robustly inhibits the of MnTE-2-PyP on tissue sparing and functional of fibronectin delivered acutely robustly inhibits the recovery. Twenty-four adult, female rats development of mechanical allodynia (but not recovery. Twenty-four adult, female rats development of mechanical allodynia (but not recovery. Twenty-four adult, female rats development of mechanical allodynia (but not received a moderately severe crush SCI at thermal hyperalgesia) over an extensive received a moderately severe crush SCI at thermal hyperalgesia) over an extensive received a moderately severe crush SCI at thermal hyperalgesia) over an extensive T10calibrated forceps. MnTE-2-PyP (1mg/kg) observation period following spinal cord dorsal T10calibrated forceps. MnTE-2-PyP (1mg/kg) observation period following spinal cord dorsal T10calibrated forceps. MnTE-2-PyP (1mg/kg) observation period following spinal cord dorsal or vehicle (Hanks Buffered Saline Solution) was column crush injury. By applying various or vehicle (Hanks Buffered Saline Solution) was column crush injury. By applying various or vehicle (Hanks Buffered Saline Solution) was column crush injury. By applying various

72 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 72 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 72 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO fibronectin fragments as well as competitive protocol, administered daily to adult female SD fibronectin fragments as well as competitive protocol, administered daily to adult female SD fibronectin fragments as well as competitive protocol, administered daily to adult female SD inhibitors, these effects were shown to be rats with moderate (12.5g-cm) thoracic inhibitors, these effects were shown to be rats with moderate (12.5g-cm) thoracic inhibitors, these effects were shown to be rats with moderate (12.5g-cm) thoracic dependent on the CS-1 motif of fibronectin. contusion injuries. We found that locomotor dependent on the CS-1 motif of fibronectin. contusion injuries. We found that locomotor dependent on the CS-1 motif of fibronectin. contusion injuries. We found that locomotor Furthermore, we found that acute fibronectin function was rapidly and dramatically reduced Furthermore, we found that acute fibronectin function was rapidly and dramatically reduced Furthermore, we found that acute fibronectin function was rapidly and dramatically reduced treatment diminished inflammation and blood following even a single stretching session and treatment diminished inflammation and blood following even a single stretching session and treatment diminished inflammation and blood following even a single stretching session and spinal cord barrier permeability which, in turn, that this drop in function accumulated over the spinal cord barrier permeability which, in turn, that this drop in function accumulated over the spinal cord barrier permeability which, in turn, that this drop in function accumulated over the leads to enhanced tissue and fiber sparing as first 4-5 weeks post-injury. Interestingly, the leads to enhanced tissue and fiber sparing as first 4-5 weeks post-injury. Interestingly, the leads to enhanced tissue and fiber sparing as first 4-5 weeks post-injury. Interestingly, the well as fiber sprouting. In particular, the negative impact of the stretching protocol well as fiber sprouting. In particular, the negative impact of the stretching protocol well as fiber sprouting. In particular, the negative impact of the stretching protocol reduction of 5-HT in the superficial dorsal horn, decreased at 6-8 weeks post-injury, and when reduction of 5-HT in the superficial dorsal horn, decreased at 6-8 weeks post-injury, and when reduction of 5-HT in the superficial dorsal horn, decreased at 6-8 weeks post-injury, and when an important descending brainstem system in stretching ceased at 8 weeks the majority of an important descending brainstem system in stretching ceased at 8 weeks the majority of an important descending brainstem system in stretching ceased at 8 weeks the majority of the modulation of pain, was reversed with animals showed a robust recovery but with the modulation of pain, was reversed with animals showed a robust recovery but with the modulation of pain, was reversed with animals showed a robust recovery but with fibronectin treatment. We conclude that significant retained deficits compared to fibronectin treatment. We conclude that significant retained deficits compared to fibronectin treatment. We conclude that significant retained deficits compared to treatment of SCI with fibronectin preserves unstretched controls. These observations treatment of SCI with fibronectin preserves unstretched controls. These observations treatment of SCI with fibronectin preserves unstretched controls. These observations sensory regulation and prevents the suggest that the spinal cord circuitry is sensory regulation and prevents the suggest that the spinal cord circuitry is sensory regulation and prevents the suggest that the spinal cord circuitry is development of chronic allodynia, providing a particularly vulnerable to aberrant afferent input development of chronic allodynia, providing a particularly vulnerable to aberrant afferent input development of chronic allodynia, providing a particularly vulnerable to aberrant afferent input potential therapeutic intervention to treat acutely post-injury and that every action (or potential therapeutic intervention to treat acutely post-injury and that every action (or potential therapeutic intervention to treat acutely post-injury and that every action (or chronic pain following SCI. inaction) and treatment applied to SCI patients chronic pain following SCI. inaction) and treatment applied to SCI patients chronic pain following SCI. inaction) and treatment applied to SCI patients should be considered to have consequences that should be considered to have consequences that should be considered to have consequences that P-62 Every Move You Make: Consequences may fundamentally change the trajectory of P-62 Every Move You Make: Consequences may fundamentally change the trajectory of P-62 Every Move You Make: Consequences may fundamentally change the trajectory of of A Stretching/ROM Therapy Post-SCI recovery. Supported by the Kentucky Spinal of A Stretching/ROM Therapy Post-SCI recovery. Supported by the Kentucky Spinal of A Stretching/ROM Therapy Post-SCI recovery. Supported by the Kentucky Spinal Cord and Head Injury Research Trust and by the Cord and Head Injury Research Trust and by the Cord and Head Injury Research Trust and by the K.L. Caudle, D.A. Atkinson, A. Shum-Siu, NIH/NINDS (R01 NS052292) and NIH/NCRR K.L. Caudle, D.A. Atkinson, A. Shum-Siu, NIH/NINDS (R01 NS052292) and NIH/NCRR K.L. Caudle, D.A. Atkinson, A. Shum-Siu, NIH/NINDS (R01 NS052292) and NIH/NCRR D.S.K. Magnuson (P20 RR15576). D.S.K. Magnuson (P20 RR15576). D.S.K. Magnuson (P20 RR15576). Kentucky Spinal Cord Injury Research Kentucky Spinal Cord Injury Research Kentucky Spinal Cord Injury Research Center, University of Louisville, Louisville, KY. P-63 Comparison Of The Effects Of Center, University of Louisville, Louisville, KY. P-63 Comparison Of The Effects Of Center, University of Louisville, Louisville, KY. P-63 Comparison Of The Effects Of Rubrospinal Tract And Red Nucleus Lesions Rubrospinal Tract And Red Nucleus Lesions Rubrospinal Tract And Red Nucleus Lesions A potential impediment to the translation On Skilled Reaching. A potential impediment to the translation On Skilled Reaching. A potential impediment to the translation On Skilled Reaching. of effective therapies for spinal cord injury of effective therapies for spinal cord injury of effective therapies for spinal cord injury (SCI) is that the conditions of recovery in R. Morris and A. Kearsley (SCI) is that the conditions of recovery in R. Morris and A. Kearsley (SCI) is that the conditions of recovery in R. Morris and A. Kearsley animal models to not parallel those of patients. Translational Neuroscience Facility, animal models to not parallel those of patients. Translational Neuroscience Facility, animal models to not parallel those of patients. Translational Neuroscience Facility, In contrast to rodent models that show high School of Medical Sciences, The University of In contrast to rodent models that show high School of Medical Sciences, The University of In contrast to rodent models that show high School of Medical Sciences, The University of levels of activity within a few weeks of New South Wales, Sydney, NSW, Australia. levels of activity within a few weeks of New South Wales, Sydney, NSW, Australia. levels of activity within a few weeks of New South Wales, Sydney, NSW, Australia. incomplete injuries, the majority of patients are incomplete injuries, the majority of patients are incomplete injuries, the majority of patients are largely immobile for weeks or months receiving We have recently shown that small largely immobile for weeks or months receiving We have recently shown that small largely immobile for weeks or months receiving We have recently shown that small only stretching and range-of-motion (ROM) spinal cord lesions that damage the rubrospinal only stretching and range-of-motion (ROM) spinal cord lesions that damage the rubrospinal only stretching and range-of-motion (ROM) spinal cord lesions that damage the rubrospinal therapies, which are almost universally tract (RST) while sparing the other fibre therapies, which are almost universally tract (RST) while sparing the other fibre therapies, which are almost universally tract (RST) while sparing the other fibre delivered in some form. Stretching therapy is pathways running in the lateral funiculus delivered in some form. Stretching therapy is pathways running in the lateral funiculus delivered in some form. Stretching therapy is pathways running in the lateral funiculus employed primarily to avoid peripheral tissue selectively abolish the arpeggio movement in employed primarily to avoid peripheral tissue selectively abolish the arpeggio movement in employed primarily to avoid peripheral tissue selectively abolish the arpeggio movement in pathologies, and the influence, positive or skilled reaching (Morris et al., 2011). On the pathologies, and the influence, positive or skilled reaching (Morris et al., 2011). On the pathologies, and the influence, positive or skilled reaching (Morris et al., 2011). On the negative, of stretching on spinal cord circuitry is other hand, lesions of the red nucleus (RN) have negative, of stretching on spinal cord circuitry is other hand, lesions of the red nucleus (RN) have negative, of stretching on spinal cord circuitry is other hand, lesions of the red nucleus (RN) have completely unknown. We found recently that a been shown to interfere with several aspects of completely unknown. We found recently that a been shown to interfere with several aspects of completely unknown. We found recently that a been shown to interfere with several aspects of daily stretching protocol resulted in a significant skilled reaching including the arpeggio daily stretching protocol resulted in a significant skilled reaching including the arpeggio daily stretching protocol resulted in a significant skilled reaching including the arpeggio attenuation of locomotor function following movement (Whishaw and Gorny, 1996; attenuation of locomotor function following movement (Whishaw and Gorny, 1996; attenuation of locomotor function following movement (Whishaw and Gorny, 1996; mild-moderate T9 contusions (Caudle et al., Whishaw et al., 1998). The RST is the main mild-moderate T9 contusions (Caudle et al., Whishaw et al., 1998). The RST is the main mild-moderate T9 contusions (Caudle et al., Whishaw et al., 1998). The RST is the main 2011). Thus, in the current study we utilized an descending output of the RN. Deficits in 2011). Thus, in the current study we utilized an descending output of the RN. Deficits in 2011). Thus, in the current study we utilized an descending output of the RN. Deficits in intensive, physical therapy-based stretching arpeggio after RN lesions are therefore in line intensive, physical therapy-based stretching arpeggio after RN lesions are therefore in line intensive, physical therapy-based stretching arpeggio after RN lesions are therefore in line

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 73 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 73 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 73 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO with our recent findings. However, the (PI3K)/Akt/mammalian target of rapamycin with our recent findings. However, the (PI3K)/Akt/mammalian target of rapamycin with our recent findings. However, the (PI3K)/Akt/mammalian target of rapamycin additional deficits reported after RN lesions are (mTOR) pathway which is negatively regulated additional deficits reported after RN lesions are (mTOR) pathway which is negatively regulated additional deficits reported after RN lesions are (mTOR) pathway which is negatively regulated difficult to reconcile with our recent results. The by phosphatase and tensin homolog deleted on difficult to reconcile with our recent results. The by phosphatase and tensin homolog deleted on difficult to reconcile with our recent results. The by phosphatase and tensin homolog deleted on present study was designed to compare, in the chromosome ten (PTEN). The rubrospinal tract present study was designed to compare, in the chromosome ten (PTEN). The rubrospinal tract present study was designed to compare, in the chromosome ten (PTEN). The rubrospinal tract same experimental setup, the outcomes of RN (RST), which originates in the red nucleus of same experimental setup, the outcomes of RN (RST), which originates in the red nucleus of same experimental setup, the outcomes of RN (RST), which originates in the red nucleus of lesions with that of lesions to the RST. Long the midbrain and travels contralaterally in the lesions with that of lesions to the RST. Long the midbrain and travels contralaterally in the lesions with that of lesions to the RST. Long the midbrain and travels contralaterally in the Evans female rats were trained to reach for dorsolateral funiculus of the spinal cord, is an Evans female rats were trained to reach for dorsolateral funiculus of the spinal cord, is an Evans female rats were trained to reach for dorsolateral funiculus of the spinal cord, is an single sugar pellets. After the completion of the alternative model of CNS axon regenerative single sugar pellets. After the completion of the alternative model of CNS axon regenerative single sugar pellets. After the completion of the alternative model of CNS axon regenerative training, the animals were subjected to either failure. Here, we assessed whether PTEN training, the animals were subjected to either failure. Here, we assessed whether PTEN training, the animals were subjected to either failure. Here, we assessed whether PTEN RN or RST lesions. Detailed movement analysis deletion would promote axon regeneration in the RN or RST lesions. Detailed movement analysis deletion would promote axon regeneration in the RN or RST lesions. Detailed movement analysis deletion would promote axon regeneration in the revealed that both types of lesions abolish the RST with deletion occurring in aged (7-8 month revealed that both types of lesions abolish the RST with deletion occurring in aged (7-8 month revealed that both types of lesions abolish the RST with deletion occurring in aged (7-8 month arpeggio movement. This finding supports the old) mice. Floxed PTEN mice were injected arpeggio movement. This finding supports the old) mice. Floxed PTEN mice were injected arpeggio movement. This finding supports the old) mice. Floxed PTEN mice were injected view that the arpeggio movement is under the with adeno-associated virus serotype 2 view that the arpeggio movement is under the with adeno-associated virus serotype 2 view that the arpeggio movement is under the with adeno-associated virus serotype 2 control of the RST. RN lesions, however, expressing Cre and GFP (AAV2-Cre) or GFP control of the RST. RN lesions, however, expressing Cre and GFP (AAV2-Cre) or GFP control of the RST. RN lesions, however, expressing Cre and GFP (AAV2-Cre) or GFP creates additional deficits in the grasping action. alone for control (AAV2-GFP) into the right red creates additional deficits in the grasping action. alone for control (AAV2-GFP) into the right red creates additional deficits in the grasping action. alone for control (AAV2-GFP) into the right red The results are explained in terms of the nucleus. Four weeks later, mice underwent a left The results are explained in terms of the nucleus. Four weeks later, mice underwent a left The results are explained in terms of the nucleus. Four weeks later, mice underwent a left involvement of the RN with a network of neural dorsolateral crush at cervical level C4/C5. Six involvement of the RN with a network of neural dorsolateral crush at cervical level C4/C5. Six involvement of the RN with a network of neural dorsolateral crush at cervical level C4/C5. Six structures that are directly involved in motor weeks later, mice were injected with structures that are directly involved in motor weeks later, mice were injected with structures that are directly involved in motor weeks later, mice were injected with control (e.g., motor cortex and cerebellum). In biotinylated dextran amine (BDA) into the right control (e.g., motor cortex and cerebellum). In biotinylated dextran amine (BDA) into the right control (e.g., motor cortex and cerebellum). In biotinylated dextran amine (BDA) into the right light of these anatomical considerations, it is not red nucleus to anterogradely trace the RST. Two light of these anatomical considerations, it is not red nucleus to anterogradely trace the RST. Two light of these anatomical considerations, it is not red nucleus to anterogradely trace the RST. Two surprising that lesions to the RN have a greater weeks later, mice were sacrificed. Based on surprising that lesions to the RN have a greater weeks later, mice were sacrificed. Based on surprising that lesions to the RN have a greater weeks later, mice were sacrificed. Based on impact on skilled reaching than RST lesions. independent analyses of BDA and GFP impact on skilled reaching than RST lesions. independent analyses of BDA and GFP impact on skilled reaching than RST lesions. independent analyses of BDA and GFP labelling, AAV2-Cre injected animals showed labelling, AAV2-Cre injected animals showed labelling, AAV2-Cre injected animals showed P-64 PTEN Deletion Promotes significantly decreased dieback and increased P-64 PTEN Deletion Promotes significantly decreased dieback and increased P-64 PTEN Deletion Promotes significantly decreased dieback and increased Regenerative Sprouting In The Aged regenerative sprouting of rubrospinal axons Regenerative Sprouting In The Aged regenerative sprouting of rubrospinal axons Regenerative Sprouting In The Aged regenerative sprouting of rubrospinal axons Rubrospinal Tract through the lesion site in comparison to AAV2- Rubrospinal Tract through the lesion site in comparison to AAV2- Rubrospinal Tract through the lesion site in comparison to AAV2- GFP injected animals, for up to 100µm caudal GFP injected animals, for up to 100µm caudal GFP injected animals, for up to 100µm caudal B.J. Hilton1,2 and W. Tetzlaff1,2 measured from the middle of the lesion site. Our B.J. Hilton1,2 and W. Tetzlaff1,2 measured from the middle of the lesion site. Our B.J. Hilton1,2 and W. Tetzlaff1,2 measured from the middle of the lesion site. Our 1 International Collaboration on Repair findings suggest that PI3K/Akt/mTOR activity 1 International Collaboration on Repair findings suggest that PI3K/Akt/mTOR activity 1 International Collaboration on Repair findings suggest that PI3K/Akt/mTOR activity Discoveries (ICORD), Blusson Spinal Cord is a significant determinant of rubrospinal Discoveries (ICORD), Blusson Spinal Cord is a significant determinant of rubrospinal Discoveries (ICORD), Blusson Spinal Cord is a significant determinant of rubrospinal Centre, Vancouver, BC, Canada, V5Z 1M9; 2 regenerative potential, yet advanced age may Centre, Vancouver, BC, Canada, V5Z 1M9; 2 regenerative potential, yet advanced age may Centre, Vancouver, BC, Canada, V5Z 1M9; 2 regenerative potential, yet advanced age may Department of Zoology, University of British play an important role in decreasing the ability Department of Zoology, University of British play an important role in decreasing the ability Department of Zoology, University of British play an important role in decreasing the ability Columbia, Vancouver, BC, Canada, V6T 1Z4 of RST axons to regenerate long distances. Columbia, Vancouver, BC, Canada, V6T 1Z4 of RST axons to regenerate long distances. Columbia, Vancouver, BC, Canada, V6T 1Z4 of RST axons to regenerate long distances.

The devastating motor, sensory, and P-65 Intra-Cortical Injection of AAV- The devastating motor, sensory, and P-65 Intra-Cortical Injection of AAV- The devastating motor, sensory, and P-65 Intra-Cortical Injection of AAV- autonomic dysfunction that occurs following shRNA Abrogates PTEN Expression In autonomic dysfunction that occurs following shRNA Abrogates PTEN Expression In autonomic dysfunction that occurs following shRNA Abrogates PTEN Expression In spinal cord injury is largely the result of Cortical Motoneurons spinal cord injury is largely the result of Cortical Motoneurons spinal cord injury is largely the result of Cortical Motoneurons transected central nervous system (CNS) axons transected central nervous system (CNS) axons transected central nervous system (CNS) axons failing to regenerate. Previously Park et al. G. Lewandowski1,2 and O. Steward1,2,3,4 failing to regenerate. Previously Park et al. G. Lewandowski1,2 and O. Steward1,2,3,4 failing to regenerate. Previously Park et al. G. Lewandowski1,2 and O. Steward1,2,3,4 (Science 322, 963-966 [2008]) and Liu et al. 1Reeve-Irvine Research Center and (Science 322, 963-966 [2008]) and Liu et al. 1Reeve-Irvine Research Center and (Science 322, 963-966 [2008]) and Liu et al. 1Reeve-Irvine Research Center and (Nat Neurosci 13, 1075-1081[2010]) have Departments of 2Anatomy and Neurobiology, (Nat Neurosci 13, 1075-1081[2010]) have Departments of 2Anatomy and Neurobiology, (Nat Neurosci 13, 1075-1081[2010]) have Departments of 2Anatomy and Neurobiology, shown that a major contributor to this 3Neurobiology and Behavior, and shown that a major contributor to this 3Neurobiology and Behavior, and shown that a major contributor to this 3Neurobiology and Behavior, and regenerative failure is a diminished intrinsic 4Neurosurgery, University of California at regenerative failure is a diminished intrinsic 4Neurosurgery, University of California at regenerative failure is a diminished intrinsic 4Neurosurgery, University of California at capacity of adult CNS (retinal ganglion cellular Irvine School of Medicine, Irvine, CA 92697- capacity of adult CNS (retinal ganglion cellular Irvine School of Medicine, Irvine, CA 92697- capacity of adult CNS (retinal ganglion cellular Irvine School of Medicine, Irvine, CA 92697- and corticospinal) axons to grow, based largely 4265 and corticospinal) axons to grow, based largely 4265 and corticospinal) axons to grow, based largely 4265 on inactivity in the phosphoinositide 3-kinase on inactivity in the phosphoinositide 3-kinase on inactivity in the phosphoinositide 3-kinase

74 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 74 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 74 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

Recent studies have shown that inhibit PTEN expression in cortical neurons for Recent studies have shown that inhibit PTEN expression in cortical neurons for Recent studies have shown that inhibit PTEN expression in cortical neurons for conditional genetic deletion of the tumor prolonged periods of time. conditional genetic deletion of the tumor prolonged periods of time. conditional genetic deletion of the tumor prolonged periods of time. suppressor gene PTEN in cortical motoneurons suppressor gene PTEN in cortical motoneurons suppressor gene PTEN in cortical motoneurons enables them to regenerate their axons after P-66 Conditional Genetic Deletion of PTEN enables them to regenerate their axons after P-66 Conditional Genetic Deletion of PTEN enables them to regenerate their axons after P-66 Conditional Genetic Deletion of PTEN spinal cord injury (Liu et al., 2010, Nat. in the Sensorimotor Cortex Does Not Lead spinal cord injury (Liu et al., 2010, Nat. in the Sensorimotor Cortex Does Not Lead spinal cord injury (Liu et al., 2010, Nat. in the Sensorimotor Cortex Does Not Lead Neurosci. 13, 1075-1083). The experiments To Evident Motor Impairments Neurosci. 13, 1075-1083). The experiments To Evident Motor Impairments Neurosci. 13, 1075-1083). The experiments To Evident Motor Impairments utilized mice with a LoxP-flanked PTEN gene utilized mice with a LoxP-flanked PTEN gene utilized mice with a LoxP-flanked PTEN gene (PTENff mice), which allows local conditional K.G. Sharp1, L.E. Butler1, O.Steward1,2 (PTENff mice), which allows local conditional K.G. Sharp1, L.E. Butler1, O.Steward1,2 (PTENff mice), which allows local conditional K.G. Sharp1, L.E. Butler1, O.Steward1,2 genetic deletion of PTEN via injections of Reeve-Irvine Research Center, genetic deletion of PTEN via injections of Reeve-Irvine Research Center, genetic deletion of PTEN via injections of Reeve-Irvine Research Center, AAV-Cre. Here, our goal is to develop an 2Departments of Anatomy & Neurobiology, AAV-Cre. Here, our goal is to develop an 2Departments of Anatomy & Neurobiology, AAV-Cre. Here, our goal is to develop an 2Departments of Anatomy & Neurobiology, intervention that would allow clinically-relevant Neurobiology & Behavior, and Neurosurgery, intervention that would allow clinically-relevant Neurobiology & Behavior, and Neurosurgery, intervention that would allow clinically-relevant Neurobiology & Behavior, and Neurosurgery, proof of concept experiments in which PTEN is University of California at Irvine School of proof of concept experiments in which PTEN is University of California at Irvine School of proof of concept experiments in which PTEN is University of California at Irvine School of targeted at the time of, or after a spinal cord Medicine, Irvine, CA 92697-4265. targeted at the time of, or after a spinal cord Medicine, Irvine, CA 92697-4265. targeted at the time of, or after a spinal cord Medicine, Irvine, CA 92697-4265. injury. Towards this end we developed, in injury. Towards this end we developed, in injury. Towards this end we developed, in conjunction with the University of Pennsylvania Recent studies have shown that conjunction with the University of Pennsylvania Recent studies have shown that conjunction with the University of Pennsylvania Recent studies have shown that Vector Core, an adeno-associated virus (AAV) conditional genetic deletion of the tumor Vector Core, an adeno-associated virus (AAV) conditional genetic deletion of the tumor Vector Core, an adeno-associated virus (AAV) conditional genetic deletion of the tumor vector that expresses an shRNA specific for suppressor gene PTEN in cortical motoneurons vector that expresses an shRNA specific for suppressor gene PTEN in cortical motoneurons vector that expresses an shRNA specific for suppressor gene PTEN in cortical motoneurons PTEN (AAV2/9-shPTEN) and the ZsGreen enables them to regenerate their axons after PTEN (AAV2/9-shPTEN) and the ZsGreen enables them to regenerate their axons after PTEN (AAV2/9-shPTEN) and the ZsGreen enables them to regenerate their axons after reporter gene. Adult Sprague Dawley rats spinal cord injury (Liu et al., 2010, Nat. reporter gene. Adult Sprague Dawley rats spinal cord injury (Liu et al., 2010, Nat. reporter gene. Adult Sprague Dawley rats spinal cord injury (Liu et al., 2010, Nat. received a single injection of 1010 genome Neurosci. 13, 1075-1083). The experiments received a single injection of 1010 genome Neurosci. 13, 1075-1083). The experiments received a single injection of 1010 genome Neurosci. 13, 1075-1083). The experiments copies of either AAV2/9-shPTEN or AAV2/9- utilized mice with a LoxP-flanked PTEN gene copies of either AAV2/9-shPTEN or AAV2/9- utilized mice with a LoxP-flanked PTEN gene copies of either AAV2/9-shPTEN or AAV2/9- utilized mice with a LoxP-flanked PTEN gene shLuc (control vector), into the sensorimotor (PTENff mice), which allows local conditional shLuc (control vector), into the sensorimotor (PTENff mice), which allows local conditional shLuc (control vector), into the sensorimotor (PTENff mice), which allows local conditional cortex. Three weeks post-injection brains were genetic deletion of PTEN via injections of cortex. Three weeks post-injection brains were genetic deletion of PTEN via injections of cortex. Three weeks post-injection brains were genetic deletion of PTEN via injections of stained for H&E and immunostained for PTEN AAV-Cre. Analysis of brain sections from mice stained for H&E and immunostained for PTEN AAV-Cre. Analysis of brain sections from mice stained for H&E and immunostained for PTEN AAV-Cre. Analysis of brain sections from mice and phosphorylated ribosomal protein S6 (pS6), that received injections of AAV-Cre into the and phosphorylated ribosomal protein S6 (pS6), that received injections of AAV-Cre into the and phosphorylated ribosomal protein S6 (pS6), that received injections of AAV-Cre into the a marker for activation of mTOR-dependent sensorimotor cortex at postnatal day 1 (P1) and a marker for activation of mTOR-dependent sensorimotor cortex at postnatal day 1 (P1) and a marker for activation of mTOR-dependent sensorimotor cortex at postnatal day 1 (P1) and protein synthesis. Immunostaining for PTEN survived for 1.5 years revealed hypertrophy of protein synthesis. Immunostaining for PTEN survived for 1.5 years revealed hypertrophy of protein synthesis. Immunostaining for PTEN survived for 1.5 years revealed hypertrophy of was absent in a region approximately 500 µm in individual PTEN-deleted neurons and a was absent in a region approximately 500 µm in individual PTEN-deleted neurons and a was absent in a region approximately 500 µm in individual PTEN-deleted neurons and a diameter in AAV2/9-shPTEN injected brains in disruption of cortical lamination. Our goal here diameter in AAV2/9-shPTEN injected brains in disruption of cortical lamination. Our goal here diameter in AAV2/9-shPTEN injected brains in disruption of cortical lamination. Our goal here the same area exhibiting expression of the was to assess whether deletion of PTEN and the the same area exhibiting expression of the was to assess whether deletion of PTEN and the the same area exhibiting expression of the was to assess whether deletion of PTEN and the ZsGreen reporter. Neurons in the area of PTEN resulting anatomical changes in the cortex ZsGreen reporter. Neurons in the area of PTEN resulting anatomical changes in the cortex ZsGreen reporter. Neurons in the area of PTEN resulting anatomical changes in the cortex deletion showed increased immunostaing for disrupted motor function. PTENff mice received deletion showed increased immunostaing for disrupted motor function. PTENff mice received deletion showed increased immunostaing for disrupted motor function. PTENff mice received pS6, indicating persistent activation of mTOR- bilateral injections of AAV-Cre or AAV-GFP pS6, indicating persistent activation of mTOR- bilateral injections of AAV-Cre or AAV-GFP pS6, indicating persistent activation of mTOR- bilateral injections of AAV-Cre or AAV-GFP dependent protein synthesis. There were no into the sensorimotor cortex at P1. At 6-8 dependent protein synthesis. There were no into the sensorimotor cortex at P1. At 6-8 dependent protein synthesis. There were no into the sensorimotor cortex at P1. At 6-8 changes in immunostaining for PTEN or pS6 in months of age, mice were tested on a battery of changes in immunostaining for PTEN or pS6 in months of age, mice were tested on a battery of changes in immunostaining for PTEN or pS6 in months of age, mice were tested on a battery of AAV2/9-shLuc injected brains. Examination of motor function tasks including grip walk, ladder AAV2/9-shLuc injected brains. Examination of motor function tasks including grip walk, ladder AAV2/9-shLuc injected brains. Examination of motor function tasks including grip walk, ladder H&E stained sections revealed hypertrophy of climb, grid walk, Basso Mouse Scale (BMS), H&E stained sections revealed hypertrophy of climb, grid walk, Basso Mouse Scale (BMS), H&E stained sections revealed hypertrophy of climb, grid walk, Basso Mouse Scale (BMS), individual PTEN-deleted neurons, but no overt rotarod and open field exploratory activity. individual PTEN-deleted neurons, but no overt rotarod and open field exploratory activity. individual PTEN-deleted neurons, but no overt rotarod and open field exploratory activity. cytotoxicty or other pathology. Finally, during Overall, motor performance of mice that cytotoxicty or other pathology. Finally, during Overall, motor performance of mice that cytotoxicty or other pathology. Finally, during Overall, motor performance of mice that the 3 weeks after AAV2/9-shPTEN injection, received bilateral AAV-Cre or AAV-GFP the 3 weeks after AAV2/9-shPTEN injection, received bilateral AAV-Cre or AAV-GFP the 3 weeks after AAV2/9-shPTEN injection, received bilateral AAV-Cre or AAV-GFP we did not observe any adverse effects on injections was comparable to age-matched we did not observe any adverse effects on injections was comparable to age-matched we did not observe any adverse effects on injections was comparable to age-matched normal rat behaviors including activity, eating control mice. The only differences were that normal rat behaviors including activity, eating control mice. The only differences were that normal rat behaviors including activity, eating control mice. The only differences were that and grooming. These findings represent a PTEN-deleted mice had impaired performance and grooming. These findings represent a PTEN-deleted mice had impaired performance and grooming. These findings represent a PTEN-deleted mice had impaired performance preliminary indication that AAV2/9-shPTEN on the rotarod, although differences were not preliminary indication that AAV2/9-shPTEN on the rotarod, although differences were not preliminary indication that AAV2/9-shPTEN on the rotarod, although differences were not can be used to efficaciously and specifically statistically significant. These findings represent can be used to efficaciously and specifically statistically significant. These findings represent can be used to efficaciously and specifically statistically significant. These findings represent a preliminary test of the safety of long-term a preliminary test of the safety of long-term a preliminary test of the safety of long-term

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 75 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 75 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 75 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO deletion of PTEN, and reveal that the absence of especially neurons in layers III-IV. Neurons deletion of PTEN, and reveal that the absence of especially neurons in layers III-IV. Neurons deletion of PTEN, and reveal that the absence of especially neurons in layers III-IV. Neurons PTEN in cortical neurons and the resulting lacking PTEN showed increased PTEN in cortical neurons and the resulting lacking PTEN showed increased PTEN in cortical neurons and the resulting lacking PTEN showed increased alterations in cortical morphology have no immunostaining for phospho-S6, indicating alterations in cortical morphology have no immunostaining for phospho-S6, indicating alterations in cortical morphology have no immunostaining for phospho-S6, indicating adverse effects on gross motor function. persistent activation of mTOR-dependent adverse effects on gross motor function. persistent activation of mTOR-dependent adverse effects on gross motor function. persistent activation of mTOR-dependent protein synthesis. Examination of H&E stained protein synthesis. Examination of H&E stained protein synthesis. Examination of H&E stained P-67 Long-Term Deletion of PTEN in the sections revealed substantial hypertrophy of P-67 Long-Term Deletion of PTEN in the sections revealed substantial hypertrophy of P-67 Long-Term Deletion of PTEN in the sections revealed substantial hypertrophy of Sensorimotor Cortex Causes Neuronal neurons, especially pyramidal neurons in layer Sensorimotor Cortex Causes Neuronal neurons, especially pyramidal neurons in layer Sensorimotor Cortex Causes Neuronal neurons, especially pyramidal neurons in layer Hypertrophy But Does Not Lead To Tumors V and a disruption of normal cortical Hypertrophy But Does Not Lead To Tumors V and a disruption of normal cortical Hypertrophy But Does Not Lead To Tumors V and a disruption of normal cortical Or Other Neuropathology lamination, in part because neurons in layer III Or Other Neuropathology lamination, in part because neurons in layer III Or Other Neuropathology lamination, in part because neurons in layer III and IV were less tightly packed. Importantly, and IV were less tightly packed. Importantly, and IV were less tightly packed. Importantly, M.M. Buyukozturk1,2,5, B. Brandon5, O. there was no evidence of tumors or other M.M. Buyukozturk1,2,5, B. Brandon5, O. there was no evidence of tumors or other M.M. Buyukozturk1,2,5, B. Brandon5, O. there was no evidence of tumors or other Steward1,2,3,4,5 cellular pathology. These findings represent a Steward1,2,3,4,5 cellular pathology. These findings represent a Steward1,2,3,4,5 cellular pathology. These findings represent a 1Reeve-Irvine Research Center and preliminary test of the safety of long term PTEN 1Reeve-Irvine Research Center and preliminary test of the safety of long term PTEN 1Reeve-Irvine Research Center and preliminary test of the safety of long term PTEN Departments of 2Anatomy and Neurobiology, deletion, and reveal that long term deletion Departments of 2Anatomy and Neurobiology, deletion, and reveal that long term deletion Departments of 2Anatomy and Neurobiology, deletion, and reveal that long term deletion 3Neurobiology and Behavior, and causes no obvious neuropathology. 3Neurobiology and Behavior, and causes no obvious neuropathology. 3Neurobiology and Behavior, and causes no obvious neuropathology. 4Neurosurgery, 5School of Medicine, University 4Neurosurgery, 5School of Medicine, University 4Neurosurgery, 5School of Medicine, University of California, Irvine P-68 3D Imaging Of CST Axons That of California, Irvine P-68 3D Imaging Of CST Axons That of California, Irvine P-68 3D Imaging Of CST Axons That Regenerate After Spinal Cord Injury Due To Regenerate After Spinal Cord Injury Due To Regenerate After Spinal Cord Injury Due To Recent studies reveal that conditional PTEN Deletion Recent studies reveal that conditional PTEN Deletion Recent studies reveal that conditional PTEN Deletion genetic deletion of the tumor suppressor gene genetic deletion of the tumor suppressor gene genetic deletion of the tumor suppressor gene PTEN in CNS neurons induces a capacity for R. Willenberg1,2, A. Ertürk3,4, F. Bradke3,5, Z. PTEN in CNS neurons induces a capacity for R. Willenberg1,2, A. Ertürk3,4, F. Bradke3,5, Z. PTEN in CNS neurons induces a capacity for R. Willenberg1,2, A. Ertürk3,4, F. Bradke3,5, Z. robust axon regeneration. The experiments took He6, and O. Steward1,2,7,8 robust axon regeneration. The experiments took He6, and O. Steward1,2,7,8 robust axon regeneration. The experiments took He6, and O. Steward1,2,7,8 advantage of mice with a LoxP-flanked PTEN 1Reeve-Irvine Research Center, and advantage of mice with a LoxP-flanked PTEN 1Reeve-Irvine Research Center, and advantage of mice with a LoxP-flanked PTEN 1Reeve-Irvine Research Center, and gene (PTRENff mice), which allows local 2Departments of Anatomy and Neurobiology, gene (PTRENff mice), which allows local 2Departments of Anatomy and Neurobiology, gene (PTRENff mice), which allows local 2Departments of Anatomy and Neurobiology, conditional genetic deletion of PTEN via 7Neurobiology and Behavior, and conditional genetic deletion of PTEN via 7Neurobiology and Behavior, and conditional genetic deletion of PTEN via 7Neurobiology and Behavior, and injections of AAV-Cre. Mature mice that 8Neurosurgery, University of California at injections of AAV-Cre. Mature mice that 8Neurosurgery, University of California at injections of AAV-Cre. Mature mice that 8Neurosurgery, University of California at received AAV-Cre injections into the Irvine School of Medicine, Irvine, California received AAV-Cre injections into the Irvine School of Medicine, Irvine, California received AAV-Cre injections into the Irvine School of Medicine, Irvine, California sensorimotor cortex at postnatal day 1 (P1) 92697, USA; 3Axonal Growth and sensorimotor cortex at postnatal day 1 (P1) 92697, USA; 3Axonal Growth and sensorimotor cortex at postnatal day 1 (P1) 92697, USA; 3Axonal Growth and exhibited robust regeneration of CST axons Regeneration, Max Planck Institute of exhibited robust regeneration of CST axons Regeneration, Max Planck Institute of exhibited robust regeneration of CST axons Regeneration, Max Planck Institute of after spinal cord injury as adults (Liu et al., Neurobiology, Am Klopferspitz 18, 82152 after spinal cord injury as adults (Liu et al., Neurobiology, Am Klopferspitz 18, 82152 after spinal cord injury as adults (Liu et al., Neurobiology, Am Klopferspitz 18, 82152 2010, Nat. Neurosci. 13, 1075-1083). An Martinsried, Germany 2010, Nat. Neurosci. 13, 1075-1083). An Martinsried, Germany 2010, Nat. Neurosci. 13, 1075-1083). An Martinsried, Germany important consideration for potential translation 4Department of Neuroscience, Genentech, South important consideration for potential translation 4Department of Neuroscience, Genentech, South important consideration for potential translation 4Department of Neuroscience, Genentech, South is that PTEN is a tumor suppressor gene. Here, San Francisco, CA 94080, USA is that PTEN is a tumor suppressor gene. Here, San Francisco, CA 94080, USA is that PTEN is a tumor suppressor gene. Here, San Francisco, CA 94080, USA we assess whether deletion of PTEN in the 5 German Center for Neurodegenerative we assess whether deletion of PTEN in the 5 German Center for Neurodegenerative we assess whether deletion of PTEN in the 5 German Center for Neurodegenerative cortex causes tumors or other neuropathology. Diseases (DZNE), Axon Growth and cortex causes tumors or other neuropathology. Diseases (DZNE), Axon Growth and cortex causes tumors or other neuropathology. Diseases (DZNE), Axon Growth and PTENff mice received intracortical AAV-Cre Regeneration, Ludwig-Erhard-Allee 2, 53175 PTENff mice received intracortical AAV-Cre Regeneration, Ludwig-Erhard-Allee 2, 53175 PTENff mice received intracortical AAV-Cre Regeneration, Ludwig-Erhard-Allee 2, 53175 injections at birth and were allowed to survive Bonn, Germany; 6F.M. Kirby Neurobiology injections at birth and were allowed to survive Bonn, Germany; 6F.M. Kirby Neurobiology injections at birth and were allowed to survive Bonn, Germany; 6F.M. Kirby Neurobiology for 1.5 years. Brains were stained for H&E and Center, Children's Hospital, and Department of for 1.5 years. Brains were stained for H&E and Center, Children's Hospital, and Department of for 1.5 years. Brains were stained for H&E and Center, Children's Hospital, and Department of immunostained for PTEN and phosphorylated Neurology, Harvard Medical School, Boston, immunostained for PTEN and phosphorylated Neurology, Harvard Medical School, Boston, immunostained for PTEN and phosphorylated Neurology, Harvard Medical School, Boston, ribosomal protein S6 (pS6), a marker for MA, USA ribosomal protein S6 (pS6), a marker for MA, USA ribosomal protein S6 (pS6), a marker for MA, USA activation of mTOR-dependent protein activation of mTOR-dependent protein activation of mTOR-dependent protein synthesis. Immunostaining revealed that many A recent study has shown that deletion synthesis. Immunostaining revealed that many A recent study has shown that deletion synthesis. Immunostaining revealed that many A recent study has shown that deletion cortical neurons lacked PTEN including large of PTEN in the sensorimotor cortex enables cortical neurons lacked PTEN including large of PTEN in the sensorimotor cortex enables cortical neurons lacked PTEN including large of PTEN in the sensorimotor cortex enables pyramidal neurons in layer V (the cells of origin robust regeneration of corticospinal tract (CST) pyramidal neurons in layer V (the cells of origin robust regeneration of corticospinal tract (CST) pyramidal neurons in layer V (the cells of origin robust regeneration of corticospinal tract (CST) of the corticospinal tract). Some neurons in the axons beyond a spinal cord lesion (Liu et al., of the corticospinal tract). Some neurons in the axons beyond a spinal cord lesion (Liu et al., of the corticospinal tract). Some neurons in the axons beyond a spinal cord lesion (Liu et al., injected area remained PTEN positive, Nature Neuroscience 13, 1075-1081, 2010). injected area remained PTEN positive, Nature Neuroscience 13, 1075-1081, 2010). injected area remained PTEN positive, Nature Neuroscience 13, 1075-1081, 2010).

76 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 76 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 76 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

Importantly, however, this study did not define of California, San Francisco; 2Department of Importantly, however, this study did not define of California, San Francisco; 2Department of Importantly, however, this study did not define of California, San Francisco; 2Department of the origin of regenerating axons, course, and Psychology, Texas A&M University the origin of regenerating axons, course, and Psychology, Texas A&M University the origin of regenerating axons, course, and Psychology, Texas A&M University degree of midline crossing for individual axons. degree of midline crossing for individual axons. degree of midline crossing for individual axons. To address these questions, we have employed a Recovery of function after spinal cord To address these questions, we have employed a Recovery of function after spinal cord To address these questions, we have employed a Recovery of function after spinal cord technique for imaging fluorescently labeled injury (SCI) is hindered by the expression of a technique for imaging fluorescently labeled injury (SCI) is hindered by the expression of a technique for imaging fluorescently labeled injury (SCI) is hindered by the expression of a axons in unsectioned blocks of spinal cord host of neuroinflammatory agents. These agents axons in unsectioned blocks of spinal cord host of neuroinflammatory agents. These agents axons in unsectioned blocks of spinal cord host of neuroinflammatory agents. These agents (Ertürk et al., Nature Medicine, in press). Mice can induce neuropathic pain states, drive (Ertürk et al., Nature Medicine, in press). Mice can induce neuropathic pain states, drive (Ertürk et al., Nature Medicine, in press). Mice can induce neuropathic pain states, drive homozygous for the floxed PTEN gene (PTEN excitotoxicity, and exacerbate cell death homozygous for the floxed PTEN gene (PTEN excitotoxicity, and exacerbate cell death homozygous for the floxed PTEN gene (PTEN excitotoxicity, and exacerbate cell death f/f) received bilateral intracortical injections of following injury. In doing so, they may also f/f) received bilateral intracortical injections of following injury. In doing so, they may also f/f) received bilateral intracortical injections of following injury. In doing so, they may also AAV-Cre at P1 to delete PTEN from cortical undermine adaptive plasticity in the spinal cord, AAV-Cre at P1 to delete PTEN from cortical undermine adaptive plasticity in the spinal cord, AAV-Cre at P1 to delete PTEN from cortical undermine adaptive plasticity in the spinal cord, motoneurons. At maturity, mice received dorsal a process essential for behavioral recovery. motoneurons. At maturity, mice received dorsal a process essential for behavioral recovery. motoneurons. At maturity, mice received dorsal a process essential for behavioral recovery. hemisection lesions at T12 to cut the dorsal and Among these inflammatory mediators, we have hemisection lesions at T12 to cut the dorsal and Among these inflammatory mediators, we have hemisection lesions at T12 to cut the dorsal and Among these inflammatory mediators, we have dorsolateral CST. After 2, 6 or 10 weeks, found that tumor necrosis factor alpha (TNFa) dorsolateral CST. After 2, 6 or 10 weeks, found that tumor necrosis factor alpha (TNFa) dorsolateral CST. After 2, 6 or 10 weeks, found that tumor necrosis factor alpha (TNFa) fluorescent mini-ruby BDA was injected into plays a major role in stunting the potential for fluorescent mini-ruby BDA was injected into plays a major role in stunting the potential for fluorescent mini-ruby BDA was injected into plays a major role in stunting the potential for the left sensorimotor cortex to trace descending rehabilitation. We have recently shown that the left sensorimotor cortex to trace descending rehabilitation. We have recently shown that the left sensorimotor cortex to trace descending rehabilitation. We have recently shown that CST axons, and mice were transcardially injury-induced release of TNFa acts to increase CST axons, and mice were transcardially injury-induced release of TNFa acts to increase CST axons, and mice were transcardially injury-induced release of TNFa acts to increase perfused 2 weeks later. Un-sectioned spinal membrane expression of calcium-permeable perfused 2 weeks later. Un-sectioned spinal membrane expression of calcium-permeable perfused 2 weeks later. Un-sectioned spinal membrane expression of calcium-permeable cords were cut into blocks and made optically AMPA receptors (CP-AMPARs), and that this cords were cut into blocks and made optically AMPA receptors (CP-AMPARs), and that this cords were cut into blocks and made optically AMPA receptors (CP-AMPARs), and that this clear for imaging with 2-photon microscopy. mechanism leads to glutamatergic excitotoxicity clear for imaging with 2-photon microscopy. mechanism leads to glutamatergic excitotoxicity clear for imaging with 2-photon microscopy. mechanism leads to glutamatergic excitotoxicity Here, we present initial observations. Rostral to and cell death. We wondered if this same Here, we present initial observations. Rostral to and cell death. We wondered if this same Here, we present initial observations. Rostral to and cell death. We wondered if this same the lesion, there is a great burst of growth mechanism may be working to inhibit adaptive the lesion, there is a great burst of growth mechanism may be working to inhibit adaptive the lesion, there is a great burst of growth mechanism may be working to inhibit adaptive emanating from the region of cut axon ends. Of spinal plasticity as well. Using a high- emanating from the region of cut axon ends. Of spinal plasticity as well. Using a high- emanating from the region of cut axon ends. Of spinal plasticity as well. Using a high- axons extending caudally, many turn away throughput behavioral model of spinal learning, axons extending caudally, many turn away throughput behavioral model of spinal learning, axons extending caudally, many turn away throughput behavioral model of spinal learning, perpendicularly at the lesion margin, some cross we were able to assess the role of TNFa, as well perpendicularly at the lesion margin, some cross we were able to assess the role of TNFa, as well perpendicularly at the lesion margin, some cross we were able to assess the role of TNFa, as well the midline, some extend into the lesion, and as how TNF might interact with CP-AMPARs, the midline, some extend into the lesion, and as how TNF might interact with CP-AMPARs, the midline, some extend into the lesion, and as how TNF might interact with CP-AMPARs, some continue farther into the caudal intact grey in affecting spinal plasticity. Using spinally some continue farther into the caudal intact grey in affecting spinal plasticity. Using spinally some continue farther into the caudal intact grey in affecting spinal plasticity. Using spinally matter. Of those continuing into caudal grey transected rat subjects, we have previously matter. Of those continuing into caudal grey transected rat subjects, we have previously matter. Of those continuing into caudal grey transected rat subjects, we have previously matter, some have axonal swellings apposed to shown that TNFa is necessary and sufficient to matter, some have axonal swellings apposed to shown that TNFa is necessary and sufficient to matter, some have axonal swellings apposed to shown that TNFa is necessary and sufficient to individual somata, suggestive of synaptic create a spinal learning deficit. In the current set individual somata, suggestive of synaptic create a spinal learning deficit. In the current set individual somata, suggestive of synaptic create a spinal learning deficit. In the current set contacts. These results indicate that axons that of experiments, we delivered intermittent contacts. These results indicate that axons that of experiments, we delivered intermittent contacts. These results indicate that axons that of experiments, we delivered intermittent regenerate due to PTEN deletion can originate nociceptive stimulation that is known to regenerate due to PTEN deletion can originate nociceptive stimulation that is known to regenerate due to PTEN deletion can originate nociceptive stimulation that is known to near cut axon ends, extend both ipsilateral and undermine spinal learning, and found that this near cut axon ends, extend both ipsilateral and undermine spinal learning, and found that this near cut axon ends, extend both ipsilateral and undermine spinal learning, and found that this contraletaral to cut parent axons, and that the regimen increased TNFa mRNA and protein contraletaral to cut parent axons, and that the regimen increased TNFa mRNA and protein contraletaral to cut parent axons, and that the regimen increased TNFa mRNA and protein lesion margin clearly remains a major barrier to expression. Further, treatment with a specific lesion margin clearly remains a major barrier to expression. Further, treatment with a specific lesion margin clearly remains a major barrier to expression. Further, treatment with a specific regenerating axons. CP-AMPAR antagonist (Naspm) prior to regenerating axons. CP-AMPAR antagonist (Naspm) prior to regenerating axons. CP-AMPAR antagonist (Naspm) prior to instrumental testing rescued the capacity for instrumental testing rescued the capacity for instrumental testing rescued the capacity for P-69 TNFa-Induced AMPA Receptor spinal learning in subjects that had been given P-69 TNFa-Induced AMPA Receptor spinal learning in subjects that had been given P-69 TNFa-Induced AMPA Receptor spinal learning in subjects that had been given Changes Undermine Adaptive Spinal exogenous TNFa or intermittent stimulation. Changes Undermine Adaptive Spinal exogenous TNFa or intermittent stimulation. Changes Undermine Adaptive Spinal exogenous TNFa or intermittent stimulation. Plasticity These behavioral and biochemical findings Plasticity These behavioral and biochemical findings Plasticity These behavioral and biochemical findings indicate that TNFa may undermine adaptive indicate that TNFa may undermine adaptive indicate that TNFa may undermine adaptive J.R. Huie1, E.D. Stuck1, K.H. Lee2, J.C. spinal plasticity after injury by inducing changes J.R. Huie1, E.D. Stuck1, K.H. Lee2, J.C. spinal plasticity after injury by inducing changes J.R. Huie1, E.D. Stuck1, K.H. Lee2, J.C. spinal plasticity after injury by inducing changes Bresnahan1, M.S. Beattie1, J.W. Grau2, A.R. in CP-AMPAR expression. Confocal Bresnahan1, M.S. Beattie1, J.W. Grau2, A.R. in CP-AMPAR expression. Confocal Bresnahan1, M.S. Beattie1, J.W. Grau2, A.R. in CP-AMPAR expression. Confocal Ferguson1 microscopy is now being employed to further Ferguson1 microscopy is now being employed to further Ferguson1 microscopy is now being employed to further 1Brain and Spinal Injury Center, assess the localization of possible CP-AMPAR 1Brain and Spinal Injury Center, assess the localization of possible CP-AMPAR 1Brain and Spinal Injury Center, assess the localization of possible CP-AMPAR Department of Neurological Surgery, University changes induced by intermittent stimulation. Department of Neurological Surgery, University changes induced by intermittent stimulation. Department of Neurological Surgery, University changes induced by intermittent stimulation.

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 77 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 77 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 77 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

P-70 An In Vitro Study Of The Roles Of addition to neurite outgrowth inhibition. Cells P-70 An In Vitro Study Of The Roles Of addition to neurite outgrowth inhibition. Cells P-70 An In Vitro Study Of The Roles Of addition to neurite outgrowth inhibition. Cells Cspgs On Neurons: Neurite Outgrowth often formed clusters in the CSPG-treated group Cspgs On Neurons: Neurite Outgrowth often formed clusters in the CSPG-treated group Cspgs On Neurons: Neurite Outgrowth often formed clusters in the CSPG-treated group Inhibition Or Neuroprotection? because of poor adhesion. However, if cells had Inhibition Or Neuroprotection? because of poor adhesion. However, if cells had Inhibition Or Neuroprotection? because of poor adhesion. However, if cells had first been allowed to adhere on PLL for 1 day first been allowed to adhere on PLL for 1 day first been allowed to adhere on PLL for 1 day P. Yu, Y. Katagiri, J. Yi, H.M. Geller before soluble CSPG was added, there was no P. Yu, Y. Katagiri, J. Yi, H.M. Geller before soluble CSPG was added, there was no P. Yu, Y. Katagiri, J. Yi, H.M. Geller before soluble CSPG was added, there was no Developmental Neurobiology Section, obvious cell loss but CSPGs significantly Developmental Neurobiology Section, obvious cell loss but CSPGs significantly Developmental Neurobiology Section, obvious cell loss but CSPGs significantly National Heart, Lung and Blood Institute, NIH, inhibited neurite outgrowth. Surprisingly, National Heart, Lung and Blood Institute, NIH, inhibited neurite outgrowth. Surprisingly, National Heart, Lung and Blood Institute, NIH, inhibited neurite outgrowth. Surprisingly, Bethesda, MD 20892 although a relatively low concentration of Bethesda, MD 20892 although a relatively low concentration of Bethesda, MD 20892 although a relatively low concentration of CSPGs (1 μg/mL immobilized or soluble CSPGs (1 μg/mL immobilized or soluble CSPGs (1 μg/mL immobilized or soluble Chondroitin sulfate proteoglycans CSPGs) showed short term (24 hour) inhibition Chondroitin sulfate proteoglycans CSPGs) showed short term (24 hour) inhibition Chondroitin sulfate proteoglycans CSPGs) showed short term (24 hour) inhibition (CSPGs) have long been known as a class of of neurite outgrowth, neurons growing on low (CSPGs) have long been known as a class of of neurite outgrowth, neurons growing on low (CSPGs) have long been known as a class of of neurite outgrowth, neurons growing on low neurite outgrowth inhibitors enriched in the glial concentration of CSPGs survived for longer neurite outgrowth inhibitors enriched in the glial concentration of CSPGs survived for longer neurite outgrowth inhibitors enriched in the glial concentration of CSPGs survived for longer scar that prevent axonal regeneration after times (when cultured for longer than 5 days) scar that prevent axonal regeneration after times (when cultured for longer than 5 days) scar that prevent axonal regeneration after times (when cultured for longer than 5 days) central nervous system (CNS) injury. Although than those on PLL. Our results collectively central nervous system (CNS) injury. Although than those on PLL. Our results collectively central nervous system (CNS) injury. Although than those on PLL. Our results collectively many studies from different groups have shown suggest that (1) high concentration of CSPGs many studies from different groups have shown suggest that (1) high concentration of CSPGs many studies from different groups have shown suggest that (1) high concentration of CSPGs that CSPGs inhibit neurite outgrowth in vitro which would inhibit cell adhesion is not that CSPGs inhibit neurite outgrowth in vitro which would inhibit cell adhesion is not that CSPGs inhibit neurite outgrowth in vitro which would inhibit cell adhesion is not using different types of neuronal cell culture recommend to be used for neurite outgrowth using different types of neuronal cell culture recommend to be used for neurite outgrowth using different types of neuronal cell culture recommend to be used for neurite outgrowth systems, it is difficult to relate the assay; (2) although CSPG accumulation at the systems, it is difficult to relate the assay; (2) although CSPG accumulation at the systems, it is difficult to relate the assay; (2) although CSPG accumulation at the concentrations used in culture to the situation in injury prevent axons from regeneration, a low concentrations used in culture to the situation in injury prevent axons from regeneration, a low concentrations used in culture to the situation in injury prevent axons from regeneration, a low vivo after injury. It is also noteworthy that the level of CSPG presented in the extracellular vivo after injury. It is also noteworthy that the level of CSPG presented in the extracellular vivo after injury. It is also noteworthy that the level of CSPG presented in the extracellular chondroitin sulfate glycosaminoglycan chains matrix might play a beneficial role in neuronal chondroitin sulfate glycosaminoglycan chains matrix might play a beneficial role in neuronal chondroitin sulfate glycosaminoglycan chains matrix might play a beneficial role in neuronal attached to the core protein of CSPGs are highly survival. attached to the core protein of CSPGs are highly survival. attached to the core protein of CSPGs are highly survival. negatively charged and would hence affect cell negatively charged and would hence affect cell negatively charged and would hence affect cell adhesion when used as a the cell culture P-71 RPTP DEMONSTRATES A adhesion when used as a the cell culture P-71 RPTP DEMONSTRATES A adhesion when used as a the cell culture P-71 RPTP DEMONSTRATES A substrate in vitro. Under these circumstances, COMPLEX PATTERN OF BINDING TO substrate in vitro. Under these circumstances, COMPLEX PATTERN OF BINDING TO substrate in vitro. Under these circumstances, COMPLEX PATTERN OF BINDING TO even though obvious neurite outgrowth PROTEOGLYCANS FOLLOWING even though obvious neurite outgrowth PROTEOGLYCANS FOLLOWING even though obvious neurite outgrowth PROTEOGLYCANS FOLLOWING inhibition is obtained it may not represent the TRAUMATIC BRAIN INJURY inhibition is obtained it may not represent the TRAUMATIC BRAIN INJURY inhibition is obtained it may not represent the TRAUMATIC BRAIN INJURY true neurite growth inhibitory activity of true neurite growth inhibitory activity of true neurite growth inhibitory activity of CSPGs. Here, using cerebellar granule neuron J. Yi1,2, Y. Katagiri 1, A. J. Symes2, and H. M. CSPGs. Here, using cerebellar granule neuron J. Yi1,2, Y. Katagiri 1, A. J. Symes2, and H. M. CSPGs. Here, using cerebellar granule neuron J. Yi1,2, Y. Katagiri 1, A. J. Symes2, and H. M. cultures, we evaluated the effects of different Geller1. cultures, we evaluated the effects of different Geller1. cultures, we evaluated the effects of different Geller1. concentrations of both immobilized and soluble 1Developmental Neurobiology Section, concentrations of both immobilized and soluble 1Developmental Neurobiology Section, concentrations of both immobilized and soluble 1Developmental Neurobiology Section, CSPGs on neuronal growth. For immobilized National Institutes of Health, Bethesda, MD CSPGs on neuronal growth. For immobilized National Institutes of Health, Bethesda, MD CSPGs on neuronal growth. For immobilized National Institutes of Health, Bethesda, MD CSPGs, at concentrations higher than 4 μg/mL, 20892, USA; 2Center for Neuroscience and CSPGs, at concentrations higher than 4 μg/mL, 20892, USA; 2Center for Neuroscience and CSPGs, at concentrations higher than 4 μg/mL, 20892, USA; 2Center for Neuroscience and many cells failed to adhere, resulting in a Regenerative Medicine, and Department of many cells failed to adhere, resulting in a Regenerative Medicine, and Department of many cells failed to adhere, resulting in a Regenerative Medicine, and Department of dramatic loss of cells. Although a strong Pharmacology, Uniformed Services University dramatic loss of cells. Although a strong Pharmacology, Uniformed Services University dramatic loss of cells. Although a strong Pharmacology, Uniformed Services University inhibition of neurite outgrowth was observed by of the Health Sciences, Bethesda, Maryland inhibition of neurite outgrowth was observed by of the Health Sciences, Bethesda, Maryland inhibition of neurite outgrowth was observed by of the Health Sciences, Bethesda, Maryland measuring the neurite length of cells that 20814 measuring the neurite length of cells that 20814 measuring the neurite length of cells that 20814 adhered to the CSPG substrates, this could also adhered to the CSPG substrates, this could also adhered to the CSPG substrates, this could also be due to a lower cell density and/or poorer Receptor protein tyrosine phosphatase be due to a lower cell density and/or poorer Receptor protein tyrosine phosphatase be due to a lower cell density and/or poorer Receptor protein tyrosine phosphatase adhesion. A relative low concentration of sigma (RPTP) is a type IIa receptor protein adhesion. A relative low concentration of sigma (RPTP) is a type IIa receptor protein adhesion. A relative low concentration of sigma (RPTP) is a type IIa receptor protein CSPGs (1 μg/mL) showed no obvious tyrosine phosphatase that plays an important CSPGs (1 μg/mL) showed no obvious tyrosine phosphatase that plays an important CSPGs (1 μg/mL) showed no obvious tyrosine phosphatase that plays an important difference in cell density compared to neurons role in neural development and after injury to difference in cell density compared to neurons role in neural development and after injury to difference in cell density compared to neurons role in neural development and after injury to plated on PLL, but neurite length was inhibited the central nervous system. Recent reports have plated on PLL, but neurite length was inhibited the central nervous system. Recent reports have plated on PLL, but neurite length was inhibited the central nervous system. Recent reports have about 30-40 %. High concentration of soluble provided data for RPTP as the neuronal about 30-40 %. High concentration of soluble provided data for RPTP as the neuronal about 30-40 %. High concentration of soluble provided data for RPTP as the neuronal CSPGs (10 μg/mL), when added at the time of receptor for chondroitin sulfate proteoglycans CSPGs (10 μg/mL), when added at the time of receptor for chondroitin sulfate proteoglycans CSPGs (10 μg/mL), when added at the time of receptor for chondroitin sulfate proteoglycans cell plating, also effected cell adhesion in (CSPGs), major axon repelling components in cell plating, also effected cell adhesion in (CSPGs), major axon repelling components in cell plating, also effected cell adhesion in (CSPGs), major axon repelling components in

78 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 78 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 78 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO the glial scar. Targeting RPTP may be an ideal partners following TBI. [Supported by the the glial scar. Targeting RPTP may be an ideal partners following TBI. [Supported by the the glial scar. Targeting RPTP may be an ideal partners following TBI. [Supported by the approach to make surviving neurons overcome Center for Neuroscience and Regenerative approach to make surviving neurons overcome Center for Neuroscience and Regenerative approach to make surviving neurons overcome Center for Neuroscience and Regenerative the barrier represented by CSPG in the glial Medicine, Uniformed Services University the barrier represented by CSPG in the glial Medicine, Uniformed Services University the barrier represented by CSPG in the glial Medicine, Uniformed Services University scar, and reduce neuronal die back in the Health Sciences, and National Heart Lung and scar, and reduce neuronal die back in the Health Sciences, and National Heart Lung and scar, and reduce neuronal die back in the Health Sciences, and National Heart Lung and periphery of injury. We therefore sought to Blood Institute, NIH] periphery of injury. We therefore sought to Blood Institute, NIH] periphery of injury. We therefore sought to Blood Institute, NIH] better understand the role of RPTP in the better understand the role of RPTP in the better understand the role of RPTP in the response to traumatic brain injury (TBI) by P-72 Reduction of CSPGs after Cortical response to traumatic brain injury (TBI) by P-72 Reduction of CSPGs after Cortical response to traumatic brain injury (TBI) by P-72 Reduction of CSPGs after Cortical using a RPTP receptor affinity probe (RAP) Brain Injury Enhances Forelimb-Evoked using a RPTP receptor affinity probe (RAP) Brain Injury Enhances Forelimb-Evoked using a RPTP receptor affinity probe (RAP) Brain Injury Enhances Forelimb-Evoked assay. Controlled cortical impact injury of mild Brain Activation assay. Controlled cortical impact injury of mild Brain Activation assay. Controlled cortical impact injury of mild Brain Activation to moderate severity was performed over the left to moderate severity was performed over the left to moderate severity was performed over the left sensory motor cortex in mice. Brains were M. Nogueira, D. Verley, D. Hovda, R. Sutton, sensory motor cortex in mice. Brains were M. Nogueira, D. Verley, D. Hovda, R. Sutton, sensory motor cortex in mice. Brains were M. Nogueira, D. Verley, D. Hovda, R. Sutton, transcardially perfused and serially sectioned for N. Harris transcardially perfused and serially sectioned for N. Harris transcardially perfused and serially sectioned for N. Harris RAP assay and immunohistochemistry at 1, 3, 7 UCLA Brain Injury Research Center, RAP assay and immunohistochemistry at 1, 3, 7 UCLA Brain Injury Research Center, RAP assay and immunohistochemistry at 1, 3, 7 UCLA Brain Injury Research Center, and 28 days post injury (dpi). cDNA Department of Neurosurgery, UCLA, Los and 28 days post injury (dpi). cDNA Department of Neurosurgery, UCLA, Los and 28 days post injury (dpi). cDNA Department of Neurosurgery, UCLA, Los corresponding to the extracellular domain of Angeles, CA, USA corresponding to the extracellular domain of Angeles, CA, USA corresponding to the extracellular domain of Angeles, CA, USA mouse RPTP was subcloned into the mouse RPTP was subcloned into the mouse RPTP was subcloned into the pAPTAG5 vector and transfected into BHK Removal of the axon-growth inhibitory pAPTAG5 vector and transfected into BHK Removal of the axon-growth inhibitory pAPTAG5 vector and transfected into BHK Removal of the axon-growth inhibitory cells. Secreted RPTP-AP fusion protein was chondroitin-sulphate-proteoglycans (CSPGs) cells. Secreted RPTP-AP fusion protein was chondroitin-sulphate-proteoglycans (CSPGs) cells. Secreted RPTP-AP fusion protein was chondroitin-sulphate-proteoglycans (CSPGs) purified by immobilized metal affinity around the glial scar after brain injury enhances purified by immobilized metal affinity around the glial scar after brain injury enhances purified by immobilized metal affinity around the glial scar after brain injury enhances chromatography (IMAC) column and used for neuronal sprouting and leads to some behavioral chromatography (IMAC) column and used for neuronal sprouting and leads to some behavioral chromatography (IMAC) column and used for neuronal sprouting and leads to some behavioral the RAP assay on brain sections. In the improvements. We assessed whether reductions the RAP assay on brain sections. In the improvements. We assessed whether reductions the RAP assay on brain sections. In the improvements. We assessed whether reductions uninjured mouse cerebral cortex, RPTP-AP in CSPGs results in improved brain activation, uninjured mouse cerebral cortex, RPTP-AP in CSPGs results in improved brain activation, uninjured mouse cerebral cortex, RPTP-AP in CSPGs results in improved brain activation, bound mainly to neuronal cell bodies with little as assessed indirectly by immediate-early-gene bound mainly to neuronal cell bodies with little as assessed indirectly by immediate-early-gene bound mainly to neuronal cell bodies with little as assessed indirectly by immediate-early-gene or no binding to perineuronal nets. Some c-FOS expression. Following controlled- or no binding to perineuronal nets. Some c-FOS expression. Following controlled- or no binding to perineuronal nets. Some c-FOS expression. Following controlled- binding was also observed on meninges and cortical-impact-injury over the left, cortical binding was also observed on meninges and cortical-impact-injury over the left, cortical binding was also observed on meninges and cortical-impact-injury over the left, cortical forelimb region in adult, male rats, forelimb region in adult, male rats, forelimb region in adult, male rats, choroid plexus. Following TBI, RPTP-AP choroid plexus. Following TBI, RPTP-AP choroid plexus. Following TBI, RPTP-AP chondroitinase-ABC (1.5µl,48U/µl) or vehicle chondroitinase-ABC (1.5µl,48U/µl) or vehicle chondroitinase-ABC (1.5µl,48U/µl) or vehicle binding was transiently observed on the blood binding was transiently observed on the blood binding was transiently observed on the blood (n=6,8) was infused immediately and at 3-days (n=6,8) was infused immediately and at 3-days (n=6,8) was infused immediately and at 3-days vessels located in the proximity to the impact vessels located in the proximity to the impact vessels located in the proximity to the impact post-injury into the injury site. At 7-days, all post-injury into the injury site. At 7-days, all post-injury into the injury site. At 7-days, all core as early as 1 dpi, which persisted up to 7 core as early as 1 dpi, which persisted up to 7 core as early as 1 dpi, which persisted up to 7 rats and a group of naïve rats (n=6) received rats and a group of naïve rats (n=6) received rats and a group of naïve rats (n=6) received dpi. RPTP-AP binding to neurons as well as dpi. RPTP-AP binding to neurons as well as dpi. RPTP-AP binding to neurons as well as right forepaw, electrical stimulation (3.5mA) for right forepaw, electrical stimulation (3.5mA) for right forepaw, electrical stimulation (3.5mA) for blood vessels was displaced by 0.5 M NaCl, blood vessels was displaced by 0.5 M NaCl, blood vessels was displaced by 0.5 M NaCl, 60mins under medetomidine sedation 60mins under medetomidine sedation 60mins under medetomidine sedation suggesting the ionic nature of the interaction. suggesting the ionic nature of the interaction. suggesting the ionic nature of the interaction. (0.1mg/kg/hr). Rats were perfused-fixed (0.1mg/kg/hr). Rats were perfused-fixed (0.1mg/kg/hr). Rats were perfused-fixed The binding was also interrupted in the presence The binding was also interrupted in the presence The binding was also interrupted in the presence 120mins after the end of the stimulation period 120mins after the end of the stimulation period 120mins after the end of the stimulation period of EDTA, demonstrating the dependency on of EDTA, demonstrating the dependency on of EDTA, demonstrating the dependency on and processed for c-FOS immunohistochemistry and processed for c-FOS immunohistochemistry and processed for c-FOS immunohistochemistry divalent metal ion for the interaction. In divalent metal ion for the interaction. In divalent metal ion for the interaction. In to determine sensory-motor cortex c-FOS+ cell to determine sensory-motor cortex c-FOS+ cell to determine sensory-motor cortex c-FOS+ cell addition, RPTP-AP binding was completely counts. Four additional groups, naïve, injured, addition, RPTP-AP binding was completely counts. Four additional groups, naïve, injured, addition, RPTP-AP binding was completely counts. Four additional groups, naïve, injured, displaceable by heparin, and partially displaced injured+vehicle and injured+chondroitinase displaceable by heparin, and partially displaced injured+vehicle and injured+chondroitinase displaceable by heparin, and partially displaced injured+vehicle and injured+chondroitinase with 15 times more concentrated CS, suggesting were not stimulated (n=3/group). Injury resulted with 15 times more concentrated CS, suggesting were not stimulated (n=3/group). Injury resulted with 15 times more concentrated CS, suggesting were not stimulated (n=3/group). Injury resulted a comparatively weaker interaction with CSPGs. in increased numbers of c-FOS+ cells, even a comparatively weaker interaction with CSPGs. in increased numbers of c-FOS+ cells, even a comparatively weaker interaction with CSPGs. in increased numbers of c-FOS+ cells, even The labeling of blood vessels by RPTP-AP without forelimb stimulation in ipsilesional grey The labeling of blood vessels by RPTP-AP without forelimb stimulation in ipsilesional grey The labeling of blood vessels by RPTP-AP without forelimb stimulation in ipsilesional grey following TBI spatio-temporally overlapped matter (GM), and bilaterally in white matter following TBI spatio-temporally overlapped matter (GM), and bilaterally in white matter following TBI spatio-temporally overlapped matter (GM), and bilaterally in white matter with increased perlecan expression following (WM) compared to naïve (P<0.05), possibly with increased perlecan expression following (WM) compared to naïve (P<0.05), possibly with increased perlecan expression following (WM) compared to naïve (P<0.05), possibly TBI, suggesting it to be the likely partner for indicating abnormal brain activity. This effect TBI, suggesting it to be the likely partner for indicating abnormal brain activity. This effect TBI, suggesting it to be the likely partner for indicating abnormal brain activity. This effect RPTP binding on the blood vessels of injured was reduced by chondroitinase infusion in WM RPTP binding on the blood vessels of injured was reduced by chondroitinase infusion in WM RPTP binding on the blood vessels of injured was reduced by chondroitinase infusion in WM cerebral cortex. These results demonstrate a but not GM in non-stimulated, injured rats (P cerebral cortex. These results demonstrate a but not GM in non-stimulated, injured rats (P cerebral cortex. These results demonstrate a but not GM in non-stimulated, injured rats (P complex binding pattern of RPTP to multiple complex binding pattern of RPTP to multiple complex binding pattern of RPTP to multiple

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 79 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 79 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 79 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

<0.01). Forelimb stimulation in injured/ effectively degrade CSPGs and thereby <0.01). Forelimb stimulation in injured/ effectively degrade CSPGs and thereby <0.01). Forelimb stimulation in injured/ effectively degrade CSPGs and thereby injured+vehicle rats significantly increased attenuate inhibition of sensory axons in a model injured+vehicle rats significantly increased attenuate inhibition of sensory axons in a model injured+vehicle rats significantly increased attenuate inhibition of sensory axons in a model ipsilesional-GM c-FOS+ cell density when of axon regeneration in vitro. To address this ipsilesional-GM c-FOS+ cell density when of axon regeneration in vitro. To address this ipsilesional-GM c-FOS+ cell density when of axon regeneration in vitro. To address this compared to contralateral or naïve values and hypothesis, we transfected Human Embryonic compared to contralateral or naïve values and hypothesis, we transfected Human Embryonic compared to contralateral or naïve values and hypothesis, we transfected Human Embryonic compared to unstimulated (P<0.05), consistent Kidney (HEK293T) cells with an ADAMTS-4- compared to unstimulated (P<0.05), consistent Kidney (HEK293T) cells with an ADAMTS-4- compared to unstimulated (P<0.05), consistent Kidney (HEK293T) cells with an ADAMTS-4- with cortical activation. Ipsilesional-WM values FLAG expression construct. The resulting with cortical activation. Ipsilesional-WM values FLAG expression construct. The resulting with cortical activation. Ipsilesional-WM values FLAG expression construct. The resulting were not different to either contralateral injured, aggrecanase, purified using FLAG-tag antibody were not different to either contralateral injured, aggrecanase, purified using FLAG-tag antibody were not different to either contralateral injured, aggrecanase, purified using FLAG-tag antibody stimulated-naïve or even non-stimulated injured affinity column chromatography, and analyzed stimulated-naïve or even non-stimulated injured affinity column chromatography, and analyzed stimulated-naïve or even non-stimulated injured affinity column chromatography, and analyzed rats, indicating no specific effect of brain using the Pierce BCA assay, SDS-PAGE, and rats, indicating no specific effect of brain using the Pierce BCA assay, SDS-PAGE, and rats, indicating no specific effect of brain using the Pierce BCA assay, SDS-PAGE, and activation. Forelimb stimulation in Western blotting, will be used for activity assays activation. Forelimb stimulation in Western blotting, will be used for activity assays activation. Forelimb stimulation in Western blotting, will be used for activity assays injured+chondroitinase treated rats resulted in in vitro. The results thus far show that injured+chondroitinase treated rats resulted in in vitro. The results thus far show that injured+chondroitinase treated rats resulted in in vitro. The results thus far show that >5-fold ipsilesional-GM c-FOS+ cell counts ADAMTS-4 can be successfully produced by >5-fold ipsilesional-GM c-FOS+ cell counts ADAMTS-4 can be successfully produced by >5-fold ipsilesional-GM c-FOS+ cell counts ADAMTS-4 can be successfully produced by compared to stimulated-injured-vehicle rats transfecting HEK293T with an expression compared to stimulated-injured-vehicle rats transfecting HEK293T with an expression compared to stimulated-injured-vehicle rats transfecting HEK293T with an expression (P<0.001). WM values were also significantly vector. The expressed ADAMTS-4-FLAG (P<0.001). WM values were also significantly vector. The expressed ADAMTS-4-FLAG (P<0.001). WM values were also significantly vector. The expressed ADAMTS-4-FLAG increased bilaterally (P<0.01). Importantly, both fusion protein can be identified by its reactivity increased bilaterally (P<0.01). Importantly, both fusion protein can be identified by its reactivity increased bilaterally (P<0.01). Importantly, both fusion protein can be identified by its reactivity GM and WM values were significantly with antibodies to the FLAG epitope, and to the GM and WM values were significantly with antibodies to the FLAG epitope, and to the GM and WM values were significantly with antibodies to the FLAG epitope, and to the increased from non-stimulated, chondroitinase- ADAMTS-4 protein itself. ADAMTS-4 was increased from non-stimulated, chondroitinase- ADAMTS-4 protein itself. ADAMTS-4 was increased from non-stimulated, chondroitinase- ADAMTS-4 protein itself. ADAMTS-4 was infused rats, indicating that c-FOS expression retained in the cell layer, and was not in the infused rats, indicating that c-FOS expression retained in the cell layer, and was not in the infused rats, indicating that c-FOS expression retained in the cell layer, and was not in the was specific to brain activation. These data media. Once purification is complete, enzymatic was specific to brain activation. These data media. Once purification is complete, enzymatic was specific to brain activation. These data media. Once purification is complete, enzymatic indicate that reduction of pericontusional activity will be assessed by the enzyme’s ability indicate that reduction of pericontusional activity will be assessed by the enzyme’s ability indicate that reduction of pericontusional activity will be assessed by the enzyme’s ability CSPGs has a significant effect on sensorimotor to degrade purified aggrecan in vitro, and CSPGs has a significant effect on sensorimotor to degrade purified aggrecan in vitro, and CSPGs has a significant effect on sensorimotor to degrade purified aggrecan in vitro, and function, and this might underlie functional outgrowth assays on degraded aggrecan in vitro function, and this might underlie functional outgrowth assays on degraded aggrecan in vitro function, and this might underlie functional outgrowth assays on degraded aggrecan in vitro recovery in this model. will be undertaken. Alone or in combination recovery in this model. will be undertaken. Alone or in combination recovery in this model. will be undertaken. Alone or in combination Support: NINDS NS055910 and UCLA Brain with other CSPG degradative proteins, Support: NINDS NS055910 and UCLA Brain with other CSPG degradative proteins, Support: NINDS NS055910 and UCLA Brain with other CSPG degradative proteins, Injury Research Center. ADAMTS-4 could become a useful therapy to Injury Research Center. ADAMTS-4 could become a useful therapy to Injury Research Center. ADAMTS-4 could become a useful therapy to selectively degrade CSPGs that inhibit neuronal selectively degrade CSPGs that inhibit neuronal selectively degrade CSPGs that inhibit neuronal P-73 Transient Expression And outgrowth thereby promoting regeneration and P-73 Transient Expression And outgrowth thereby promoting regeneration and P-73 Transient Expression And outgrowth thereby promoting regeneration and Purification Of Aggrecanase (Adamts-4) recovery of function in SCI patients. [Support: Purification Of Aggrecanase (Adamts-4) recovery of function in SCI patients. [Support: Purification Of Aggrecanase (Adamts-4) recovery of function in SCI patients. [Support: From Hek293t Cells NIH (R01 NS053470), the Department of From Hek293t Cells NIH (R01 NS053470), the Department of From Hek293t Cells NIH (R01 NS053470), the Department of Defense (W81XWH-10-1-0778; the UK Office of Defense (W81XWH-10-1-0778; the UK Office of Defense (W81XWH-10-1-0778; the UK Office of J. Davies, D. M. Snow*, and T. M. Hering* Undergraduate Research, and AMSTEMM]. * J. Davies, D. M. Snow*, and T. M. Hering* Undergraduate Research, and AMSTEMM]. * J. Davies, D. M. Snow*, and T. M. Hering* Undergraduate Research, and AMSTEMM]. * The University of Kentucky, Spinal Cord These authors contributed equally to this work. The University of Kentucky, Spinal Cord These authors contributed equally to this work. The University of Kentucky, Spinal Cord These authors contributed equally to this work. and Brain Injury Research Center, Lexington, and Brain Injury Research Center, Lexington, and Brain Injury Research Center, Lexington, KY 40536. P-74 HEK293T Cells Produce KY 40536. P-74 HEK293T Cells Produce KY 40536. P-74 HEK293T Cells Produce Proteoglycans with Varied Sulfation Proteoglycans with Varied Sulfation Proteoglycans with Varied Sulfation Following spinal cord injury (SCI), Patterns, Express Multiple Carbohydrate Following spinal cord injury (SCI), Patterns, Express Multiple Carbohydrate Following spinal cord injury (SCI), Patterns, Express Multiple Carbohydrate chondroitin sulfate proteoglycans (CSPGs, e.g. Sulfotransferases, and are a Novel System for chondroitin sulfate proteoglycans (CSPGs, e.g. Sulfotransferases, and are a Novel System for chondroitin sulfate proteoglycans (CSPGs, e.g. Sulfotransferases, and are a Novel System for aggrecan), are up-regulated and constitute a the Production of “Designer PGs”. aggrecan), are up-regulated and constitute a the Production of “Designer PGs”. aggrecan), are up-regulated and constitute a the Production of “Designer PGs”. major component of an inhibitory extracellular major component of an inhibitory extracellular major component of an inhibitory extracellular matrix (ECM). The influence of this complex J. A. Beller, T. M. Hering*, D.M. Snow* matrix (ECM). The influence of this complex J. A. Beller, T. M. Hering*, D.M. Snow* matrix (ECM). The influence of this complex J. A. Beller, T. M. Hering*, D.M. Snow* barrier must be overcome to promote neuronal Spinal Cord and Brain Injury Research barrier must be overcome to promote neuronal Spinal Cord and Brain Injury Research barrier must be overcome to promote neuronal Spinal Cord and Brain Injury Research regeneration. The aggrecanase ADAMTS-4, a Center, and Anatomy and Neurobiology, regeneration. The aggrecanase ADAMTS-4, a Center, and Anatomy and Neurobiology, regeneration. The aggrecanase ADAMTS-4, a Center, and Anatomy and Neurobiology, member of the ADAMTS (A Disintegrin And University of Kentucky, 40536. member of the ADAMTS (A Disintegrin And University of Kentucky, 40536. member of the ADAMTS (A Disintegrin And University of Kentucky, 40536. Metalloprotease with ThromboSpondin motifs) Metalloprotease with ThromboSpondin motifs) Metalloprotease with ThromboSpondin motifs) family of proteases, is capable of degrading Following spinal cord injury (SCI), the family of proteases, is capable of degrading Following spinal cord injury (SCI), the family of proteases, is capable of degrading Following spinal cord injury (SCI), the CSPGs. Our hypothesis is: ADAMTS-4 can development of a glial scar and reactive CSPGs. Our hypothesis is: ADAMTS-4 can development of a glial scar and reactive CSPGs. Our hypothesis is: ADAMTS-4 can development of a glial scar and reactive

80 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 80 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 80 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO astrocytosis results in increased expression of P-75 Overlapping Yet Distinct Roles Of astrocytosis results in increased expression of P-75 Overlapping Yet Distinct Roles Of astrocytosis results in increased expression of P-75 Overlapping Yet Distinct Roles Of chondroitin sulfate proteoglycans (CSPGs) and Matrix Metalloproteinases-2 And -9 In chondroitin sulfate proteoglycans (CSPGs) and Matrix Metalloproteinases-2 And -9 In chondroitin sulfate proteoglycans (CSPGs) and Matrix Metalloproteinases-2 And -9 In subsequent inhibition of neuronal regeneration. Modulating Angiogenesis In The Injured subsequent inhibition of neuronal regeneration. Modulating Angiogenesis In The Injured subsequent inhibition of neuronal regeneration. Modulating Angiogenesis In The Injured The sulfation pattern of CSPG-associated Spinal Cord The sulfation pattern of CSPG-associated Spinal Cord The sulfation pattern of CSPG-associated Spinal Cord glycosaminoglycans (GAGs) plays a pivotal glycosaminoglycans (GAGs) plays a pivotal glycosaminoglycans (GAGs) plays a pivotal role in neurite inhibition. In the present study, A. A. Trivedi, PhD1 , H. Zhang, PhD1, A role in neurite inhibition. In the present study, A. A. Trivedi, PhD1 , H. Zhang, PhD1, A role in neurite inhibition. In the present study, A. A. Trivedi, PhD1 , H. Zhang, PhD1, A we have developed a model to examine the Ekeledo, BA1, S. M. Lee PhD1, Z. Werb, PhD2, we have developed a model to examine the Ekeledo, BA1, S. M. Lee PhD1, Z. Werb, PhD2, we have developed a model to examine the Ekeledo, BA1, S. M. Lee PhD1, Z. Werb, PhD2, biosynthesis of CSPGs with varying sulfation K. Topp, PhD3, and L. J. Noble-Haeusslein, biosynthesis of CSPGs with varying sulfation K. Topp, PhD3, and L. J. Noble-Haeusslein, biosynthesis of CSPGs with varying sulfation K. Topp, PhD3, and L. J. Noble-Haeusslein, patterns. Human Embryonic Kidney (HEK) PhD1, 3 patterns. Human Embryonic Kidney (HEK) PhD1, 3 patterns. Human Embryonic Kidney (HEK) PhD1, 3 293T cells were transiently transfected with the 1Department of Neurosurgery, University 293T cells were transiently transfected with the 1Department of Neurosurgery, University 293T cells were transiently transfected with the 1Department of Neurosurgery, University gene for bovine aggrecan (pBAGG71-28). of California, San Francisco, California 94143 gene for bovine aggrecan (pBAGG71-28). of California, San Francisco, California 94143 gene for bovine aggrecan (pBAGG71-28). of California, San Francisco, California 94143 Through G50-Sephadex column USA; 2Department of Anatomy, University of Through G50-Sephadex column USA; 2Department of Anatomy, University of Through G50-Sephadex column USA; 2Department of Anatomy, University of chromatography and DEAE column elution, California, San Francisco, California 94143 chromatography and DEAE column elution, California, San Francisco, California 94143 chromatography and DEAE column elution, California, San Francisco, California 94143 several peaks were detected using a DMMB USA; 3Physical Therapy and Rehab Sciences, several peaks were detected using a DMMB USA; 3Physical Therapy and Rehab Sciences, several peaks were detected using a DMMB USA; 3Physical Therapy and Rehab Sciences, assay to detect total proteoglycan. The presence University of California, San Francisco, assay to detect total proteoglycan. The presence University of California, San Francisco, assay to detect total proteoglycan. The presence University of California, San Francisco, of aggrecan within these peaks was verified by California 94143 USA of aggrecan within these peaks was verified by California 94143 USA of aggrecan within these peaks was verified by California 94143 USA dot blot with an antibody to aggrecan. The dot blot with an antibody to aggrecan. The dot blot with an antibody to aggrecan. The resulting differences in retention times for Here we investigate the roles of matrix resulting differences in retention times for Here we investigate the roles of matrix resulting differences in retention times for Here we investigate the roles of matrix aggrecan were further correlated with increasing metalloproteinases (MMP)-2 and MMP-9 in aggrecan were further correlated with increasing metalloproteinases (MMP)-2 and MMP-9 in aggrecan were further correlated with increasing metalloproteinases (MMP)-2 and MMP-9 in degrees of sulfation. This novel pattern of modulation of angiogenesis in the injured spinal degrees of sulfation. This novel pattern of modulation of angiogenesis in the injured spinal degrees of sulfation. This novel pattern of modulation of angiogenesis in the injured spinal aggrecan sulfation implicates HEK293T cells as cord. Immortalized brain-derived capillary aggrecan sulfation implicates HEK293T cells as cord. Immortalized brain-derived capillary aggrecan sulfation implicates HEK293T cells as cord. Immortalized brain-derived capillary a promising model for the continuing endothelial cells (RBCEC4) express MMP-2. a promising model for the continuing endothelial cells (RBCEC4) express MMP-2. a promising model for the continuing endothelial cells (RBCEC4) express MMP-2. development of our novel “Designer PGs” to When exposed to a MMP-2 inhibitor, development of our novel “Designer PGs” to When exposed to a MMP-2 inhibitor, development of our novel “Designer PGs” to When exposed to a MMP-2 inhibitor, study the inhibitory influence of sulfation on proliferation, migration and tube formation are study the inhibitory influence of sulfation on proliferation, migration and tube formation are study the inhibitory influence of sulfation on proliferation, migration and tube formation are neurite outgrowth. Further, RT-PCR revealed reduced, thus implicating this protease in key neurite outgrowth. Further, RT-PCR revealed reduced, thus implicating this protease in key neurite outgrowth. Further, RT-PCR revealed reduced, thus implicating this protease in key the expression of carbohydrate sulfotransferases events related to angiogenesis. To examine the the expression of carbohydrate sulfotransferases events related to angiogenesis. To examine the the expression of carbohydrate sulfotransferases events related to angiogenesis. To examine the in HEK293T cells involved in the production of role of this protease in vivo, MMP-2 knockout in HEK293T cells involved in the production of role of this protease in vivo, MMP-2 knockout in HEK293T cells involved in the production of role of this protease in vivo, MMP-2 knockout the predominant sulfation patterns of CSPGs. (KO) and wildtype (WT) mice were subjected to the predominant sulfation patterns of CSPGs. (KO) and wildtype (WT) mice were subjected to the predominant sulfation patterns of CSPGs. (KO) and wildtype (WT) mice were subjected to By targeting these individual carbohydrate spinal cord injury. Endothelial cell proliferation By targeting these individual carbohydrate spinal cord injury. Endothelial cell proliferation By targeting these individual carbohydrate spinal cord injury. Endothelial cell proliferation sulfotransferases with siRNA, “Designer PGs” was reduced in the KO relative to the WT. sulfotransferases with siRNA, “Designer PGs” was reduced in the KO relative to the WT. sulfotransferases with siRNA, “Designer PGs” was reduced in the KO relative to the WT. with varied sulfation patterns can be synthesized However, KO mice showed a transient increase with varied sulfation patterns can be synthesized However, KO mice showed a transient increase with varied sulfation patterns can be synthesized However, KO mice showed a transient increase and then analyzed for their inhibitory effect on similar to WT in anatomic measures of and then analyzed for their inhibitory effect on similar to WT in anatomic measures of and then analyzed for their inhibitory effect on similar to WT in anatomic measures of neurite outgrowth. We are currently testing vascularity, including vascular density, area and neurite outgrowth. We are currently testing vascularity, including vascular density, area and neurite outgrowth. We are currently testing vascularity, including vascular density, area and novel neurite outgrowth assays to discriminate length between 7 and 14 days followed by a novel neurite outgrowth assays to discriminate length between 7 and 14 days followed by a novel neurite outgrowth assays to discriminate length between 7 and 14 days followed by a between various sulfation patterns, and testing marked reduction at 21 days. Subsequent between various sulfation patterns, and testing marked reduction at 21 days. Subsequent between various sulfation patterns, and testing marked reduction at 21 days. Subsequent their effect on neurite inhibition. This model for decline in vascularity in the KO mice their effect on neurite inhibition. This model for decline in vascularity in the KO mice their effect on neurite inhibition. This model for decline in vascularity in the KO mice the biosynthesis of CSPG constructs will allow corresponded to an upregulation of MMP-9. To the biosynthesis of CSPG constructs will allow corresponded to an upregulation of MMP-9. To the biosynthesis of CSPG constructs will allow corresponded to an upregulation of MMP-9. To us to elucidate the mechanisms of CSPG test the hypothesis that MMP-9 compensates for us to elucidate the mechanisms of CSPG test the hypothesis that MMP-9 compensates for us to elucidate the mechanisms of CSPG test the hypothesis that MMP-9 compensates for mediated neurite inhibition, while targeting MMP-2 deficiency in supporting angiogenesis, mediated neurite inhibition, while targeting MMP-2 deficiency in supporting angiogenesis, mediated neurite inhibition, while targeting MMP-2 deficiency in supporting angiogenesis, genes of human origin, and represents a RBCEC4 cells were exposed to tumor necrosis genes of human origin, and represents a RBCEC4 cells were exposed to tumor necrosis genes of human origin, and represents a RBCEC4 cells were exposed to tumor necrosis clinically relevant approach for the development factor  (TNF) to induce MMP-9 or were clinically relevant approach for the development factor  (TNF) to induce MMP-9 or were clinically relevant approach for the development factor  (TNF) to induce MMP-9 or were of novel gene therapies. [Support: NIH R01 directly exposed to purified MMP-9. Either of novel gene therapies. [Support: NIH R01 directly exposed to purified MMP-9. Either of novel gene therapies. [Support: NIH R01 directly exposed to purified MMP-9. Either NS053470 and Kentucky Spinal Cord and Head approach yielded similar findings in these NS053470 and Kentucky Spinal Cord and Head approach yielded similar findings in these NS053470 and Kentucky Spinal Cord and Head approach yielded similar findings in these Injury Research Trust (#10-11A)]. * These activated cells. Using selective pharmacologic Injury Research Trust (#10-11A)]. * These activated cells. Using selective pharmacologic Injury Research Trust (#10-11A)]. * These activated cells. Using selective pharmacologic authors contributed equally to this work. inhibitors of MMP-9 and -2, we found that authors contributed equally to this work. inhibitors of MMP-9 and -2, we found that authors contributed equally to this work. inhibitors of MMP-9 and -2, we found that endothelial proliferation was dependent on endothelial proliferation was dependent on endothelial proliferation was dependent on

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 81 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 81 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 81 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

MMP-2, while MMP-9 modulated tube transported into axons. Further depleting ZBP1 MMP-2, while MMP-9 modulated tube transported into axons. Further depleting ZBP1 MMP-2, while MMP-9 modulated tube transported into axons. Further depleting ZBP1 formation. To determine if MMP-9 directed from adult DRG neurons, either by allelic formation. To determine if MMP-9 directed from adult DRG neurons, either by allelic formation. To determine if MMP-9 directed from adult DRG neurons, either by allelic tube formation is time-dependent, RBCEC4 deletion or by introducing a dominant negative tube formation is time-dependent, RBCEC4 deletion or by introducing a dominant negative tube formation is time-dependent, RBCEC4 deletion or by introducing a dominant negative cells were subjected to a prolonged exposure to RNA, decreases axonal regrowth from injured cells were subjected to a prolonged exposure to RNA, decreases axonal regrowth from injured cells were subjected to a prolonged exposure to RNA, decreases axonal regrowth from injured either TNF or MMP-9. Such prolonged sensory neurons, both in culture and in vivo. either TNF or MMP-9. Such prolonged sensory neurons, both in culture and in vivo. either TNF or MMP-9. Such prolonged sensory neurons, both in culture and in vivo. exposure led to vascular regression. Taken Conversely, overexpressing ZBP1 increases exposure led to vascular regression. Taken Conversely, overexpressing ZBP1 increases exposure led to vascular regression. Taken Conversely, overexpressing ZBP1 increases together, these data suggest distinct and axonal outgrowth and transport of -actin and together, these data suggest distinct and axonal outgrowth and transport of -actin and together, these data suggest distinct and axonal outgrowth and transport of -actin and overlapping roles of both these gelatinases in GAP-43. These data suggest that endogenous overlapping roles of both these gelatinases in GAP-43. These data suggest that endogenous overlapping roles of both these gelatinases in GAP-43. These data suggest that endogenous angiogenesis. Our findings further suggest that axonally targeted mRNAs compete with one angiogenesis. Our findings further suggest that axonally targeted mRNAs compete with one angiogenesis. Our findings further suggest that axonally targeted mRNAs compete with one MMP-9, expressed during the time course of another for RBP binding and axonal transport. MMP-9, expressed during the time course of another for RBP binding and axonal transport. MMP-9, expressed during the time course of another for RBP binding and axonal transport. wound healing may not only support early Consistent with this, injury-induced increase in wound healing may not only support early Consistent with this, injury-induced increase in wound healing may not only support early Consistent with this, injury-induced increase in angiogenesis but direct longer-term regression. GAP-43 transcription decreases axonal levels of angiogenesis but direct longer-term regression. GAP-43 transcription decreases axonal levels of angiogenesis but direct longer-term regression. GAP-43 transcription decreases axonal levels of As the injured spinal cord of the MMP-2 null -actin with a commensurate increase in axonal As the injured spinal cord of the MMP-2 null -actin with a commensurate increase in axonal As the injured spinal cord of the MMP-2 null -actin with a commensurate increase in axonal shows a compensatory, prolonged expression of GAP-43. Since the injury conditioning for shows a compensatory, prolonged expression of GAP-43. Since the injury conditioning for shows a compensatory, prolonged expression of GAP-43. Since the injury conditioning for MMP-9, the decline in vascularity, may be transcription of GAP-43 can accelerate axonal MMP-9, the decline in vascularity, may be transcription of GAP-43 can accelerate axonal MMP-9, the decline in vascularity, may be transcription of GAP-43 can accelerate axonal attributed to this protease. regeneration, we asked if this shift in altered attributed to this protease. regeneration, we asked if this shift in altered attributed to this protease. regeneration, we asked if this shift in altered axonal mRNA levels of GAP-43 and -actin axonal mRNA levels of GAP-43 and -actin axonal mRNA levels of GAP-43 and -actin P-76 AXONAL REGROWTH IS might affect axonal growth. Indeed, selectively P-76 AXONAL REGROWTH IS might affect axonal growth. Indeed, selectively P-76 AXONAL REGROWTH IS might affect axonal growth. Indeed, selectively REGULATED BY Mrnas COMPETING depleting or overexpressing locally synthesized REGULATED BY Mrnas COMPETING depleting or overexpressing locally synthesized REGULATED BY Mrnas COMPETING depleting or overexpressing locally synthesized FOR ZBP1. GAP-43 vs. -actin protein in DRG neurons FOR ZBP1. GAP-43 vs. -actin protein in DRG neurons FOR ZBP1. GAP-43 vs. -actin protein in DRG neurons generated distinct patterns of axonal regrowth. generated distinct patterns of axonal regrowth. generated distinct patterns of axonal regrowth. 1 2 1 1 2 1 1 2 1 JL Twiss , CJ Donnelly , M. Spillane , DE The effect of overexpression was only seen with JL Twiss , CJ Donnelly , M. Spillane , DE The effect of overexpression was only seen with JL Twiss , CJ Donnelly , M. Spillane , DE The effect of overexpression was only seen with 3 1 4 5 6 3 1 4 5 6 3 1 4 5 6 Willis , M Park , M Xu , S Yoo , GJ Bassell , axonally localizing transcripts; restricting GAP- Willis , M Park , M Xu , S Yoo , GJ Bassell , axonally localizing transcripts; restricting GAP- Willis , M Park , M Xu , S Yoo , GJ Bassell , axonally localizing transcripts; restricting GAP- 1 1 1 and G. Gallo . 43 and -actin mRNAs to the cell body using and G. Gallo . 43 and -actin mRNAs to the cell body using and G. Gallo . 43 and -actin mRNAs to the cell body using 1Drexel Univ and Drexel College of 1Drexel Univ and Drexel College of 1Drexel Univ and Drexel College of 2 the non-localizing 3’UTR of -actin mRNA had 2 the non-localizing 3’UTR of -actin mRNA had 2 the non-localizing 3’UTR of -actin mRNA had Medicine, Philadelphia, PA; University of no effect on axonal growth. These studies Medicine, Philadelphia, PA; University of no effect on axonal growth. These studies Medicine, Philadelphia, PA; University of no effect on axonal growth. These studies Delaware, Newark, DE; 3Burke Research Inst., Delaware, Newark, DE; 3Burke Research Inst., Delaware, Newark, DE; 3Burke Research Inst., 4 indicate that axonally translated -actin protein 4 indicate that axonally translated -actin protein 4 indicate that axonally translated -actin protein White Plains, NY; Philadelphia College is needed for axonal branching while axonally White Plains, NY; Philadelphia College is needed for axonal branching while axonally White Plains, NY; Philadelphia College is needed for axonal branching while axonally Osteopathic Med, Philadelphia, PA; 5Nemours Osteopathic Med, Philadelphia, PA; 5Nemours Osteopathic Med, Philadelphia, PA; 5Nemours 6 translated GAP-43 protein is needed for rapid 6 translated GAP-43 protein is needed for rapid 6 translated GAP-43 protein is needed for rapid Biomed. Res., Wilmington, DE; and, Emory unilinear growth. Biomed. Res., Wilmington, DE; and, Emory unilinear growth. Biomed. Res., Wilmington, DE; and, Emory unilinear growth. University, Atlanta, GA. University, Atlanta, GA. University, Atlanta, GA. P-77 The Pro-Synaptic Protein LAR P-77 The Pro-Synaptic Protein LAR P-77 The Pro-Synaptic Protein LAR mRNAs are actively transported into Mediates Glial Scar Induced Axonal mRNAs are actively transported into Mediates Glial Scar Induced Axonal mRNAs are actively transported into Mediates Glial Scar Induced Axonal axons of cultured neurons, where the locally Regernation Failure Following Spinal Cord axons of cultured neurons, where the locally Regernation Failure Following Spinal Cord axons of cultured neurons, where the locally Regernation Failure Following Spinal Cord synthesized proteins play a role in axonal Injury synthesized proteins play a role in axonal Injury synthesized proteins play a role in axonal Injury growth. Cues for localization of these mRNAs growth. Cues for localization of these mRNAs growth. Cues for localization of these mRNAs are inherent to the RNA, with 3’UTR structures B.T. Lang1, J.M. Cregg1, Y.L. Wang1, S. Li2, and are inherent to the RNA, with 3’UTR structures B.T. Lang1, J.M. Cregg1, Y.L. Wang1, S. Li2, and are inherent to the RNA, with 3’UTR structures B.T. Lang1, J.M. Cregg1, Y.L. Wang1, S. Li2, and bound by RNA binding proteins (RBP) typically J. Silver1 bound by RNA binding proteins (RBP) typically J. Silver1 bound by RNA binding proteins (RBP) typically J. Silver1 being responsible for axonal targeting. We 1Department of Neuroscience, Case being responsible for axonal targeting. We 1Department of Neuroscience, Case being responsible for axonal targeting. We 1Department of Neuroscience, Case recently reported that the -actin’s 3’UTR is Western Reserve University, Cleveland Ohio; recently reported that the -actin’s 3’UTR is Western Reserve University, Cleveland Ohio; recently reported that the -actin’s 3’UTR is Western Reserve University, Cleveland Ohio; sufficient for axonal localization in peripheral 2Department of Neuroscience, University of sufficient for axonal localization in peripheral 2Department of Neuroscience, University of sufficient for axonal localization in peripheral 2Department of Neuroscience, University of nerve and spinal cord axons (Willis et al., 2011). Texas Southwestern Medical Center, Dallas nerve and spinal cord axons (Willis et al., 2011). Texas Southwestern Medical Center, Dallas nerve and spinal cord axons (Willis et al., 2011). Texas Southwestern Medical Center, Dallas Interestingly, both -actin and GAP-43 mRNAs Texas. Interestingly, both -actin and GAP-43 mRNAs Texas. Interestingly, both -actin and GAP-43 mRNAs Texas. require ZBP1 for their axonal localization. require ZBP1 for their axonal localization. require ZBP1 for their axonal localization. However, this RBP is expressed at very low Regeneration of damaged axons However, this RBP is expressed at very low Regeneration of damaged axons However, this RBP is expressed at very low Regeneration of damaged axons levels in adult neurons, which limits mRNAs following spinal cord injury is complicated by levels in adult neurons, which limits mRNAs following spinal cord injury is complicated by levels in adult neurons, which limits mRNAs following spinal cord injury is complicated by

82 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 82 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 82 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO several distinct processes, with the chondroitin- 1Medical Scientist Training Program, several distinct processes, with the chondroitin- 1Medical Scientist Training Program, several distinct processes, with the chondroitin- 1Medical Scientist Training Program, sulfate proteoglycan (CSPG) rich barrier at the Mayo Graduate School, and Departments of sulfate proteoglycan (CSPG) rich barrier at the Mayo Graduate School, and Departments of sulfate proteoglycan (CSPG) rich barrier at the Mayo Graduate School, and Departments of astroglial scar being a primary impediment. In 2Neurologic Surgery, and 3Physiology and astroglial scar being a primary impediment. In 2Neurologic Surgery, and 3Physiology and astroglial scar being a primary impediment. In 2Neurologic Surgery, and 3Physiology and the weeks that follow spinal cord injury, Biomedical Engineering, Mayo Clinic, the weeks that follow spinal cord injury, Biomedical Engineering, Mayo Clinic, the weeks that follow spinal cord injury, Biomedical Engineering, Mayo Clinic, damaged axons attempt to advance into the Rochester, MN 55905 USA. 4Present address: damaged axons attempt to advance into the Rochester, MN 55905 USA. 4Present address: damaged axons attempt to advance into the Rochester, MN 55905 USA. 4Present address: lesion core only to become entrapped and Department of Pediatrics, University of lesion core only to become entrapped and Department of Pediatrics, University of lesion core only to become entrapped and Department of Pediatrics, University of stopped by the inhibitory environment. Using Colorado Anschutz Medical Campus, Aurora, stopped by the inhibitory environment. Using Colorado Anschutz Medical Campus, Aurora, stopped by the inhibitory environment. Using Colorado Anschutz Medical Campus, Aurora, an in vitro assay for glial scar mediated CO 80045 USA. an in vitro assay for glial scar mediated CO 80045 USA. an in vitro assay for glial scar mediated CO 80045 USA. inhibition and time-lapse microscopy, we inhibition and time-lapse microscopy, we inhibition and time-lapse microscopy, we showed that axons become stabilized in Chemotropic factors in the extracellular showed that axons become stabilized in Chemotropic factors in the extracellular showed that axons become stabilized in Chemotropic factors in the extracellular proteoglycan rich gradients. We recently microenvironment guide nerve growth by acting proteoglycan rich gradients. We recently microenvironment guide nerve growth by acting proteoglycan rich gradients. We recently microenvironment guide nerve growth by acting showed that the LAR family phosphatase, on the growth cone at the tip of extending showed that the LAR family phosphatase, on the growth cone at the tip of extending showed that the LAR family phosphatase, on the growth cone at the tip of extending receptor-protein tyrosine phosphatase-sigma axons. Growth cone extension requires the receptor-protein tyrosine phosphatase-sigma axons. Growth cone extension requires the receptor-protein tyrosine phosphatase-sigma axons. Growth cone extension requires the (RPTPσ), a key modulator of synapse coordination of cytoskeleton-dependent (RPTPσ), a key modulator of synapse coordination of cytoskeleton-dependent (RPTPσ), a key modulator of synapse coordination of cytoskeleton-dependent maturation, is a receptor for chondroitin sulfate membrane protrusion and dynamic adhesion to maturation, is a receptor for chondroitin sulfate membrane protrusion and dynamic adhesion to maturation, is a receptor for chondroitin sulfate membrane protrusion and dynamic adhesion to proteoglycans. Given that all three LAR family the extracellular matrix (ECM), yet how proteoglycans. Given that all three LAR family the extracellular matrix (ECM), yet how proteoglycans. Given that all three LAR family the extracellular matrix (ECM), yet how members share 99% sequence homology, we chemotropic factors regulate these events members share 99% sequence homology, we chemotropic factors regulate these events members share 99% sequence homology, we chemotropic factors regulate these events tested whether LAR, a second family member, remains an outstanding question. We tested whether LAR, a second family member, remains an outstanding question. We tested whether LAR, a second family member, remains an outstanding question. We mediated over-adhesion and stabilization of demonstrated previously that the repellent factor mediated over-adhesion and stabilization of demonstrated previously that the repellent factor mediated over-adhesion and stabilization of demonstrated previously that the repellent factor growth cones leading to regeneration failure. myelin-associated glycoprotein (MAG) triggers growth cones leading to regeneration failure. myelin-associated glycoprotein (MAG) triggers growth cones leading to regeneration failure. myelin-associated glycoprotein (MAG) triggers We show that LAR is highly upregulated in the endocytic removal of the adhesion receptor β1- We show that LAR is highly upregulated in the endocytic removal of the adhesion receptor β1- We show that LAR is highly upregulated in the endocytic removal of the adhesion receptor β1- dystrophic, but not normal, growth cone. By integrin from the growth cone surface dystrophic, but not normal, growth cone. By integrin from the growth cone surface dystrophic, but not normal, growth cone. By integrin from the growth cone surface utilizing specific small peptide inhibitors to the membrane to negatively remodel ECM utilizing specific small peptide inhibitors to the membrane to negatively remodel ECM utilizing specific small peptide inhibitors to the membrane to negatively remodel ECM intracellular domains of LAR coupled with a adhesions during chemorepulsion (Hines et al., intracellular domains of LAR coupled with a adhesions during chemorepulsion (Hines et al., intracellular domains of LAR coupled with a adhesions during chemorepulsion (Hines et al., cytosolic-localizing TAT domain, we showed 2010). Here we report that the neurotrophin cytosolic-localizing TAT domain, we showed 2010). Here we report that the neurotrophin cytosolic-localizing TAT domain, we showed 2010). Here we report that the neurotrophin that adhesion to CSPG substrate was diminished brain-derived neurotropic factor (BDNF) that adhesion to CSPG substrate was diminished brain-derived neurotropic factor (BDNF) that adhesion to CSPG substrate was diminished brain-derived neurotropic factor (BDNF) upon LAR inactivation. In addition, we show positively regulates the formation of substrate upon LAR inactivation. In addition, we show positively regulates the formation of substrate upon LAR inactivation. In addition, we show positively regulates the formation of substrate inactivation of LAR can allow a dystrophic, adhesions in axonal growth cones during inactivation of LAR can allow a dystrophic, adhesions in axonal growth cones during inactivation of LAR can allow a dystrophic, adhesions in axonal growth cones during highly adhesive growth cone to advance into a stimulated outgrowth and prevents removal of highly adhesive growth cone to advance into a stimulated outgrowth and prevents removal of highly adhesive growth cone to advance into a stimulated outgrowth and prevents removal of CSPG gradient and eventually cross the barrier. β1-integrin adhesions by MAG. Treatment of CSPG gradient and eventually cross the barrier. β1-integrin adhesions by MAG. Treatment of CSPG gradient and eventually cross the barrier. β1-integrin adhesions by MAG. Treatment of Our results suggest for the first time that CSPGs Xenopus spinal neurons with BDNF rapidly Our results suggest for the first time that CSPGs Xenopus spinal neurons with BDNF rapidly Our results suggest for the first time that CSPGs Xenopus spinal neurons with BDNF rapidly in the lesion environment block regenerative triggered β1-integrin clustering and induced the in the lesion environment block regenerative triggered β1-integrin clustering and induced the in the lesion environment block regenerative triggered β1-integrin clustering and induced the growth by creating an abnormally high adhesive dynamic formation of nascent vinculin- growth by creating an abnormally high adhesive dynamic formation of nascent vinculin- growth by creating an abnormally high adhesive dynamic formation of nascent vinculin- interaction with the substrate. Furthermore, our containing adhesion complexes in the growth interaction with the substrate. Furthermore, our containing adhesion complexes in the growth interaction with the substrate. Furthermore, our containing adhesion complexes in the growth results show that LAR can be modulated to cone periphery. Both the formation of nascent results show that LAR can be modulated to cone periphery. Both the formation of nascent results show that LAR can be modulated to cone periphery. Both the formation of nascent prevent the over-adhesion and stabilization of β1-integrin adhesions and the stimulation of prevent the over-adhesion and stabilization of β1-integrin adhesions and the stimulation of prevent the over-adhesion and stabilization of β1-integrin adhesions and the stimulation of axons following spinal cord injury, potentially axon extension by BDNF required cytoplasmic axons following spinal cord injury, potentially axon extension by BDNF required cytoplasmic axons following spinal cord injury, potentially axon extension by BDNF required cytoplasmic allowing for regeneration. Supported by Ca2+ signaling and integrin activation at the cell allowing for regeneration. Supported by Ca2+ signaling and integrin activation at the cell allowing for regeneration. Supported by Ca2+ signaling and integrin activation at the cell NINDS NS025713 to JS. surface. Exposure to MAG decreased the NINDS NS025713 to JS. surface. Exposure to MAG decreased the NINDS NS025713 to JS. surface. Exposure to MAG decreased the number of β1-integrin adhesions in the growth number of β1-integrin adhesions in the growth number of β1-integrin adhesions in the growth P-78 Bidirectional Remodeling Of 1- cone during inhibition of axon extension. In P-78 Bidirectional Remodeling Of 1- cone during inhibition of axon extension. In P-78 Bidirectional Remodeling Of 1- cone during inhibition of axon extension. In Integrin Adhesions During Chemotropic contrast, the BDNF-induced adhesions were Integrin Adhesions During Chemotropic contrast, the BDNF-induced adhesions were Integrin Adhesions During Chemotropic contrast, the BDNF-induced adhesions were Regulation Of Nerve Growth resistant to negative remodeling by MAG, Regulation Of Nerve Growth resistant to negative remodeling by MAG, Regulation Of Nerve Growth resistant to negative remodeling by MAG, correlating with the ability of BDNF correlating with the ability of BDNF correlating with the ability of BDNF L.P. Carlstrom1, J.H. Hines2,4, J.R. Henley2,3 pretreatment to overcome MAG-inhibition of L.P. Carlstrom1, J.H. Hines2,4, J.R. Henley2,3 pretreatment to overcome MAG-inhibition of L.P. Carlstrom1, J.H. Hines2,4, J.R. Henley2,3 pretreatment to overcome MAG-inhibition of axon extension. Pre-exposure to MAG axon extension. Pre-exposure to MAG axon extension. Pre-exposure to MAG

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 83 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 83 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 83 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO prevented the BDNF-induced formation of β1- response. Studies are underway to understand prevented the BDNF-induced formation of β1- response. Studies are underway to understand prevented the BDNF-induced formation of β1- response. Studies are underway to understand integrin adhesions and blocked the stimulation the possible mechanisms underlying this integrin adhesions and blocked the stimulation the possible mechanisms underlying this integrin adhesions and blocked the stimulation the possible mechanisms underlying this of axon extension by BDNF. Altogether, these location specific regenerative phenotype. of axon extension by BDNF. Altogether, these location specific regenerative phenotype. of axon extension by BDNF. Altogether, these location specific regenerative phenotype. findings demonstrate the neurotrophin- findings demonstrate the neurotrophin- findings demonstrate the neurotrophin- dependent formation of integrin-based P-80 A Very Large Organelle in dependent formation of integrin-based P-80 A Very Large Organelle in dependent formation of integrin-based P-80 A Very Large Organelle in adhesions in the growth cone and reveal how a Sympathetic Neurons adhesions in the growth cone and reveal how a Sympathetic Neurons adhesions in the growth cone and reveal how a Sympathetic Neurons positive regulator of growth cone substrate positive regulator of growth cone substrate positive regulator of growth cone substrate adhesions can block the negative remodeling D.V. Hunter and M.S. Ramer adhesions can block the negative remodeling D.V. Hunter and M.S. Ramer adhesions can block the negative remodeling D.V. Hunter and M.S. Ramer and growth inhibitory effects of MAG. International Collaboration on Repair and growth inhibitory effects of MAG. International Collaboration on Repair and growth inhibitory effects of MAG. International Collaboration on Repair Techniques for manipulating integrin Discoveries (ICORD), the University of British Techniques for manipulating integrin Discoveries (ICORD), the University of British Techniques for manipulating integrin Discoveries (ICORD), the University of British internalization and activation state may be Columbia, Vancouver, British Columbia, internalization and activation state may be Columbia, Vancouver, British Columbia, internalization and activation state may be Columbia, Vancouver, British Columbia, important for overcoming local inhibitory Canada important for overcoming local inhibitory Canada important for overcoming local inhibitory Canada factors after traumatic injury or factors after traumatic injury or factors after traumatic injury or neurodegenerative disease to enhance Recently a large, non-membranous neurodegenerative disease to enhance Recently a large, non-membranous neurodegenerative disease to enhance Recently a large, non-membranous regenerative nerve growth. Supported by the US organelle, named the loukomasome (“doughnut” regenerative nerve growth. Supported by the US organelle, named the loukomasome (“doughnut” regenerative nerve growth. Supported by the US organelle, named the loukomasome (“doughnut” National Institutes of Health (NS067311). body) was discovered within specific National Institutes of Health (NS067311). body) was discovered within specific National Institutes of Health (NS067311). body) was discovered within specific References: subpopulations of peripheral autonomic References: subpopulations of peripheral autonomic References: subpopulations of peripheral autonomic Hines JH, Abu-Rub M, and Henley JR (2010) ganglion neurons. This proteinaceous organelle Hines JH, Abu-Rub M, and Henley JR (2010) ganglion neurons. This proteinaceous organelle Hines JH, Abu-Rub M, and Henley JR (2010) ganglion neurons. This proteinaceous organelle Nat Neurosci 13:829-837. is found throughout the sympathetic chain with Nat Neurosci 13:829-837. is found throughout the sympathetic chain with Nat Neurosci 13:829-837. is found throughout the sympathetic chain with the highest proportions in the pelvic and stellate the highest proportions in the pelvic and stellate the highest proportions in the pelvic and stellate P-79 In Vivo 2 Photon Imaging Of CNS ganglia (innervating the pelvic organs and heart, P-79 In Vivo 2 Photon Imaging Of CNS ganglia (innervating the pelvic organs and heart, P-79 In Vivo 2 Photon Imaging Of CNS ganglia (innervating the pelvic organs and heart, Injury In Nogo Deficient Mice respectively). Additionally, a small population Injury In Nogo Deficient Mice respectively). Additionally, a small population Injury In Nogo Deficient Mice respectively). Additionally, a small population of neurons in the superior cervical ganglion of neurons in the superior cervical ganglion of neurons in the superior cervical ganglion A. Lorenzana, O. Ghassemi, B. Zheng (innervating the pineal gland) also contains A. Lorenzana, O. Ghassemi, B. Zheng (innervating the pineal gland) also contains A. Lorenzana, O. Ghassemi, B. Zheng (innervating the pineal gland) also contains University of California, San Diego loukoumasomes. In all cases, the University of California, San Diego loukoumasomes. In all cases, the University of California, San Diego loukoumasomes. In all cases, the Department of Neurosciences loukoumasome is restricted to neurons which Department of Neurosciences loukoumasome is restricted to neurons which Department of Neurosciences loukoumasome is restricted to neurons which co-express neuropeptide Y (NPY) and co-express neuropeptide Y (NPY) and co-express neuropeptide Y (NPY) and After CNS injury the ability to follow calbindin-D28K, indicating that target-derived After CNS injury the ability to follow calbindin-D28K, indicating that target-derived After CNS injury the ability to follow calbindin-D28K, indicating that target-derived axon dynamics after injury is difficult due to the factors common to these tissues may specify axon dynamics after injury is difficult due to the factors common to these tissues may specify axon dynamics after injury is difficult due to the factors common to these tissues may specify conventional methods used to track axons after whether a neuron contains this organelle. The conventional methods used to track axons after whether a neuron contains this organelle. The conventional methods used to track axons after whether a neuron contains this organelle. The injury. However, with the use of 2-photon loukoumasome appears singly within a neuron injury. However, with the use of 2-photon loukoumasome appears singly within a neuron injury. However, with the use of 2-photon loukoumasome appears singly within a neuron imaging and mice with fluorescently labeled in one of multiple possible conformations, imaging and mice with fluorescently labeled in one of multiple possible conformations, imaging and mice with fluorescently labeled in one of multiple possible conformations, axons, it is now possible to examine the which is dependent on its position within the axons, it is now possible to examine the which is dependent on its position within the axons, it is now possible to examine the which is dependent on its position within the behavior of axons at a high spatial and temporal cell. The three most common conformations behavior of axons at a high spatial and temporal cell. The three most common conformations behavior of axons at a high spatial and temporal cell. The three most common conformations resolution. In this study, we examine the identified are: toroidal when on the nuclear side resolution. In this study, we examine the identified are: toroidal when on the nuclear side resolution. In this study, we examine the identified are: toroidal when on the nuclear side degeneration and regeneration profiles of YFP of the trans-golgi network (TGN), twisted when degeneration and regeneration profiles of YFP of the trans-golgi network (TGN), twisted when degeneration and regeneration profiles of YFP of the trans-golgi network (TGN), twisted when labeled ascending sensory axons in Nogo on the boundary of the TGN, and rod shaped labeled ascending sensory axons in Nogo on the boundary of the TGN, and rod shaped labeled ascending sensory axons in Nogo on the boundary of the TGN, and rod shaped deficient mice. Single sensory axons were when peripheral to the TGN. Furthermore, the deficient mice. Single sensory axons were when peripheral to the TGN. Furthermore, the deficient mice. Single sensory axons were when peripheral to the TGN. Furthermore, the injured and imaged for several hours and loukoumasome associates with other organelles, injured and imaged for several hours and loukoumasome associates with other organelles, injured and imaged for several hours and loukoumasome associates with other organelles, reimaged days and weeks later. Preliminary notably the primary cilium, an important reimaged days and weeks later. Preliminary notably the primary cilium, an important reimaged days and weeks later. Preliminary notably the primary cilium, an important data suggests that there are no significant signaling centre, and the poorly understood data suggests that there are no significant signaling centre, and the poorly understood data suggests that there are no significant signaling centre, and the poorly understood differences in degeneration between the nematosome. The protein composition of the differences in degeneration between the nematosome. The protein composition of the differences in degeneration between the nematosome. The protein composition of the ascending and descending branches of single loukoumasome is also currently under ascending and descending branches of single loukoumasome is also currently under ascending and descending branches of single loukoumasome is also currently under sensory axons. However, there is a location investigation: the core is composed, at least in sensory axons. However, there is a location investigation: the core is composed, at least in sensory axons. However, there is a location investigation: the core is composed, at least in specific regeneration phenotype that suggests part, of the microtubule nucleating protein specific regeneration phenotype that suggests part, of the microtubule nucleating protein specific regeneration phenotype that suggests part, of the microtubule nucleating protein that not all injury locations will elicit the same gamma-tubulin, as well as the centrosome that not all injury locations will elicit the same gamma-tubulin, as well as the centrosome that not all injury locations will elicit the same gamma-tubulin, as well as the centrosome

84 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 84 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 84 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO associated proteins myosinIIb and cenexin, sodium and calcium electrophysiology which associated proteins myosinIIb and cenexin, sodium and calcium electrophysiology which associated proteins myosinIIb and cenexin, sodium and calcium electrophysiology which whereas the outer shell is composed of a yet leads to axonal energy depletion and calpain whereas the outer shell is composed of a yet leads to axonal energy depletion and calpain whereas the outer shell is composed of a yet leads to axonal energy depletion and calpain undefined protein. Its presence in multiple protease activation is a demonstrated axon undefined protein. Its presence in multiple protease activation is a demonstrated axon undefined protein. Its presence in multiple protease activation is a demonstrated axon subcellular compartments, interaction with the injury mechanism; and pharmacological subcellular compartments, interaction with the injury mechanism; and pharmacological subcellular compartments, interaction with the injury mechanism; and pharmacological primary cilium and association of a motor inhibition of ion channels is neuroprotective in primary cilium and association of a motor inhibition of ion channels is neuroprotective in primary cilium and association of a motor inhibition of ion channels is neuroprotective in protein implies motility though the dynamic MS animal models. These findings lead to the protein implies motility though the dynamic MS animal models. These findings lead to the protein implies motility though the dynamic MS animal models. These findings lead to the behaviour of this organelle has yet to be unifying hypothesis: cytotoxic CD8+ T cells behaviour of this organelle has yet to be unifying hypothesis: cytotoxic CD8+ T cells behaviour of this organelle has yet to be unifying hypothesis: cytotoxic CD8+ T cells defined. Characterization of all the cellular dysregulate axonal sodium and calcium defined. Characterization of all the cellular dysregulate axonal sodium and calcium defined. Characterization of all the cellular dysregulate axonal sodium and calcium components of neurons facilitates the gradients via a GzB-dependent mechanism that components of neurons facilitates the gradients via a GzB-dependent mechanism that components of neurons facilitates the gradients via a GzB-dependent mechanism that understanding of normal form and function of leads to local energy depletion, calpain understanding of normal form and function of leads to local energy depletion, calpain understanding of normal form and function of leads to local energy depletion, calpain neurons and allows for the identification of the activation and ultimately axon injury and loss. neurons and allows for the identification of the activation and ultimately axon injury and loss. neurons and allows for the identification of the activation and ultimately axon injury and loss. changes that occur upon injury and disease. Western blot data demonstrates that purified changes that occur upon injury and disease. Western blot data demonstrates that purified changes that occur upon injury and disease. Western blot data demonstrates that purified GzB effectively and specifically cleaves GzB effectively and specifically cleaves GzB effectively and specifically cleaves P-81 CD8+ T Cell Granzymes Injure Axons NaV1.2, NaV1.6 and spectrin. Preliminary data P-81 CD8+ T Cell Granzymes Injure Axons NaV1.2, NaV1.6 and spectrin. Preliminary data P-81 CD8+ T Cell Granzymes Injure Axons NaV1.2, NaV1.6 and spectrin. Preliminary data By Dysregulating Axonal Ionic Homeostasis implicates GzB activity as sufficient to By Dysregulating Axonal Ionic Homeostasis implicates GzB activity as sufficient to By Dysregulating Axonal Ionic Homeostasis implicates GzB activity as sufficient to dysregulate NaV1.6 electrophysiological dysregulate NaV1.6 electrophysiological dysregulate NaV1.6 electrophysiological B. M. Sauer1, 2 W. F. Schmastieg3, C. L. Howe1, 3, function. Finally, imaging studies establish B. M. Sauer1, 2 W. F. Schmastieg3, C. L. Howe1, 3, function. Finally, imaging studies establish B. M. Sauer1, 2 W. F. Schmastieg3, C. L. Howe1, 3, function. Finally, imaging studies establish 4 CD8+ T cells as competent to induce 4 CD8+ T cells as competent to induce 4 CD8+ T cells as competent to induce 1Mayo Clinic Molecular Neuroscience perturbations in axonal calcium gradients and 1Mayo Clinic Molecular Neuroscience perturbations in axonal calcium gradients and 1Mayo Clinic Molecular Neuroscience perturbations in axonal calcium gradients and Program, 2Mayo Clinic Medical Scientist injure axons, in vitro. Further experimental Program, 2Mayo Clinic Medical Scientist injure axons, in vitro. Further experimental Program, 2Mayo Clinic Medical Scientist injure axons, in vitro. Further experimental Training Program, 3Mayo Clinic Department of investigations are anticipated to demonstrate Training Program, 3Mayo Clinic Department of investigations are anticipated to demonstrate Training Program, 3Mayo Clinic Department of investigations are anticipated to demonstrate Neurology & 4Mayo Clinic Department of granzymes as sufficient to induce axonal sodium Neurology & 4Mayo Clinic Department of granzymes as sufficient to induce axonal sodium Neurology & 4Mayo Clinic Department of granzymes as sufficient to induce axonal sodium Immunology channel dysfunction and axonal ionic Immunology channel dysfunction and axonal ionic Immunology channel dysfunction and axonal ionic dysregulation as a mechanism by which CD8+ dysregulation as a mechanism by which CD8+ dysregulation as a mechanism by which CD8+ Multiple sclerosis (MS) is a primary T cells injure axons. These findings offer a Multiple sclerosis (MS) is a primary T cells injure axons. These findings offer a Multiple sclerosis (MS) is a primary T cells injure axons. These findings offer a cause of neurological disability for young adults novel mechanism of neuroimmunological axon cause of neurological disability for young adults novel mechanism of neuroimmunological axon cause of neurological disability for young adults novel mechanism of neuroimmunological axon in Westernized countries. MS-related functional injury and may reveal novel therapeutic in Westernized countries. MS-related functional injury and may reveal novel therapeutic in Westernized countries. MS-related functional injury and may reveal novel therapeutic deficits correlate with axon loss and CD8+ T strategies for the targeted prevention of CD8+ T deficits correlate with axon loss and CD8+ T strategies for the targeted prevention of CD8+ T deficits correlate with axon loss and CD8+ T strategies for the targeted prevention of CD8+ T cell burden in human cases and animal models. cell-driven neuropathology. cell burden in human cases and animal models. cell-driven neuropathology. cell burden in human cases and animal models. cell-driven neuropathology. Genetic deletion of CD8+ T cell target Genetic deletion of CD8+ T cell target Genetic deletion of CD8+ T cell target recognition (β2-microglobulin, an MHC-I P-82 Toll-Like Receptor 2 Activation recognition (β2-microglobulin, an MHC-I P-82 Toll-Like Receptor 2 Activation recognition (β2-microglobulin, an MHC-I P-82 Toll-Like Receptor 2 Activation component) or cytotoxic effector functions Limits Axon Dieback In Vivo And Promotes component) or cytotoxic effector functions Limits Axon Dieback In Vivo And Promotes component) or cytotoxic effector functions Limits Axon Dieback In Vivo And Promotes (perforin, of the perforin-granzyme protease Macrophage-Mediated Regeneration In Vitro (perforin, of the perforin-granzyme protease Macrophage-Mediated Regeneration In Vitro (perforin, of the perforin-granzyme protease Macrophage-Mediated Regeneration In Vitro system) is neuroprotective in a MS animal Without Causing Concurrent Neurotoxicity system) is neuroprotective in a MS animal Without Causing Concurrent Neurotoxicity system) is neuroprotective in a MS animal Without Causing Concurrent Neurotoxicity model. These observations implicate CD8+ T model. These observations implicate CD8+ T model. These observations implicate CD8+ T cells as drivers of MS-related neurological J.C. Gensel, K.A. Beckwith, and P.G. Popovich cells as drivers of MS-related neurological J.C. Gensel, K.A. Beckwith, and P.G. Popovich cells as drivers of MS-related neurological J.C. Gensel, K.A. Beckwith, and P.G. Popovich deficits; however, mechanistic linkages between The Ohio State University College of deficits; however, mechanistic linkages between The Ohio State University College of deficits; however, mechanistic linkages between The Ohio State University College of functional deficits, axon loss and CD8+ T cell Medicine, Center for Brain and Spinal Cord functional deficits, axon loss and CD8+ T cell Medicine, Center for Brain and Spinal Cord functional deficits, axon loss and CD8+ T cell Medicine, Center for Brain and Spinal Cord activity remain elusive. CD8+ T cell granzyme Repair, Department of Neuroscience. activity remain elusive. CD8+ T cell granzyme Repair, Department of Neuroscience. activity remain elusive. CD8+ T cell granzyme Repair, Department of Neuroscience. proteases cleave proteins that possess specific Columbus, OH 43210 proteases cleave proteins that possess specific Columbus, OH 43210 proteases cleave proteins that possess specific Columbus, OH 43210 amino acid recognition sequences. The axonal amino acid recognition sequences. The axonal amino acid recognition sequences. The axonal voltage-gated sodium channel isoforms, NaV1.2 Zymosan-activated macrophages voltage-gated sodium channel isoforms, NaV1.2 Zymosan-activated macrophages voltage-gated sodium channel isoforms, NaV1.2 Zymosan-activated macrophages and NaV1.6, and NaV-associated structural (ZAMs) promote regeneration of injured and NaV1.6, and NaV-associated structural (ZAMs) promote regeneration of injured and NaV1.6, and NaV-associated structural (ZAMs) promote regeneration of injured proteins ankryin G and spectrin contain peripheral and central nervous system axons but proteins ankryin G and spectrin contain peripheral and central nervous system axons but proteins ankryin G and spectrin contain peripheral and central nervous system axons but bioinformatically predicted granzyme B (GzB) also cause tissue pathology and cell death bioinformatically predicted granzyme B (GzB) also cause tissue pathology and cell death bioinformatically predicted granzyme B (GzB) also cause tissue pathology and cell death cleavage sequences. Dysregulation axonal (Gensel et al., 2009). Here, we test the cleavage sequences. Dysregulation axonal (Gensel et al., 2009). Here, we test the cleavage sequences. Dysregulation axonal (Gensel et al., 2009). Here, we test the

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 85 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 85 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 85 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO hypothesis that the divergent effects of ZAMs Miami Project to Cure Paralysis, hypothesis that the divergent effects of ZAMs Miami Project to Cure Paralysis, hypothesis that the divergent effects of ZAMs Miami Project to Cure Paralysis, are induced by the concurrent activation of toll- University of Miami, Miami, FL 33136, USA are induced by the concurrent activation of toll- University of Miami, Miami, FL 33136, USA are induced by the concurrent activation of toll- University of Miami, Miami, FL 33136, USA like receptor 2 (TLR2) and dectin-1 receptors. like receptor 2 (TLR2) and dectin-1 receptors. like receptor 2 (TLR2) and dectin-1 receptors. With the goal of uncoupling the beneficial and We propose that brainstem raphe nuclei With the goal of uncoupling the beneficial and We propose that brainstem raphe nuclei With the goal of uncoupling the beneficial and We propose that brainstem raphe nuclei detrimental effects of zymosan activation to are capable of orchestrating a spectrum of detrimental effects of zymosan activation to are capable of orchestrating a spectrum of detrimental effects of zymosan activation to are capable of orchestrating a spectrum of promote regeneration without toxicity, we protective and reparative responses in promote regeneration without toxicity, we protective and reparative responses in promote regeneration without toxicity, we protective and reparative responses in compared the effects of activating macrophages traumatized CNS regions, involving widespread compared the effects of activating macrophages traumatized CNS regions, involving widespread compared the effects of activating macrophages traumatized CNS regions, involving widespread in vivo or in vitro with selective agonists of co-release of serotonin and neuropeptides such in vivo or in vitro with selective agonists of co-release of serotonin and neuropeptides such in vivo or in vitro with selective agonists of co-release of serotonin and neuropeptides such TLR2 or dectin-1 receptors. All responses were as thyrotropin-releasing hormone (TRH), TLR2 or dectin-1 receptors. All responses were as thyrotropin-releasing hormone (TRH), TLR2 or dectin-1 receptors. All responses were as thyrotropin-releasing hormone (TRH), compared to those achieved with zymosan substance P (SP) and galanin (Gal). We here compared to those achieved with zymosan substance P (SP) and galanin (Gal). We here compared to those achieved with zymosan substance P (SP) and galanin (Gal). We here activation alone. Intraspinal microinjection of report that stimulating the hindbrain nucleus activation alone. Intraspinal microinjection of report that stimulating the hindbrain nucleus activation alone. Intraspinal microinjection of report that stimulating the hindbrain nucleus dectin-1 agonists mimicked the effects of raphe magnus (NRM) 3 days after thoracic dectin-1 agonists mimicked the effects of raphe magnus (NRM) 3 days after thoracic dectin-1 agonists mimicked the effects of raphe magnus (NRM) 3 days after thoracic zymosan, i.e., activated macrophages co- contusion acutely increased cyclic adenosine zymosan, i.e., activated macrophages co- contusion acutely increased cyclic adenosine zymosan, i.e., activated macrophages co- contusion acutely increased cyclic adenosine localized with zone of focal necrosis, overt axon monophosphate, which has several known localized with zone of focal necrosis, overt axon monophosphate, which has several known localized with zone of focal necrosis, overt axon monophosphate, which has several known pathology and demyelination. In contrast, restorative actions. The increase was blocked by pathology and demyelination. In contrast, restorative actions. The increase was blocked by pathology and demyelination. In contrast, restorative actions. The increase was blocked by intraspinal injection of Pam2CSK4, a synthetic the 5-HT7 antagonist pimozide (1 mg/kg, i.p.). intraspinal injection of Pam2CSK4, a synthetic the 5-HT7 antagonist pimozide (1 mg/kg, i.p.). intraspinal injection of Pam2CSK4, a synthetic the 5-HT7 antagonist pimozide (1 mg/kg, i.p.). TLR2 agonist, elicited a robust macrophage We further investigated this signal cascade: TLR2 agonist, elicited a robust macrophage We further investigated this signal cascade: TLR2 agonist, elicited a robust macrophage We further investigated this signal cascade: response but with significantly less axon or western blot analysis showed significant response but with significantly less axon or western blot analysis showed significant response but with significantly less axon or western blot analysis showed significant myelin pathology than zymosan or dectin-1 recovery to control levels of phosphorylated myelin pathology than zymosan or dectin-1 recovery to control levels of phosphorylated myelin pathology than zymosan or dectin-1 recovery to control levels of phosphorylated agonists. In vitro, products released by zymosan protein kinase A (p-PKA) in cervical, thoracic agonists. In vitro, products released by zymosan protein kinase A (p-PKA) in cervical, thoracic agonists. In vitro, products released by zymosan protein kinase A (p-PKA) in cervical, thoracic or Pam2CSK4-stimulated macrophages and lumbar segments after stimulation of the or Pam2CSK4-stimulated macrophages and lumbar segments after stimulation of the or Pam2CSK4-stimulated macrophages and lumbar segments after stimulation of the increased axon growth from adult DRG NRM, compared with injured non-stimulated increased axon growth from adult DRG NRM, compared with injured non-stimulated increased axon growth from adult DRG NRM, compared with injured non-stimulated neurons. Importantly, Pam2CSK4-activated animals, while PKA values were restored to neurons. Importantly, Pam2CSK4-activated animals, while PKA values were restored to neurons. Importantly, Pam2CSK4-activated animals, while PKA values were restored to macrophages promoted axon growth without control values in cervical and lumbar tissue. macrophages promoted axon growth without control values in cervical and lumbar tissue. macrophages promoted axon growth without control values in cervical and lumbar tissue. also causing toxicity. In contrast, activation of Although cAMP responsive element binding also causing toxicity. In contrast, activation of Although cAMP responsive element binding also causing toxicity. In contrast, activation of Although cAMP responsive element binding macrophages via dectin-1 caused neurotoxicity. protein (CREB) was unchanged, stimulation macrophages via dectin-1 caused neurotoxicity. protein (CREB) was unchanged, stimulation macrophages via dectin-1 caused neurotoxicity. protein (CREB) was unchanged, stimulation In vivo, Pam2CSK4 injection into the site of significantly increased p-CREB levels In vivo, Pam2CSK4 injection into the site of significantly increased p-CREB levels In vivo, Pam2CSK4 injection into the site of significantly increased p-CREB levels dorsal column crush injury significantly reduced throughout the injured cord. A high-content dorsal column crush injury significantly reduced throughout the injured cord. A high-content dorsal column crush injury significantly reduced throughout the injured cord. A high-content macrophage-mediated axonal dieback. screening platform using cultured E18 macrophage-mediated axonal dieback. screening platform using cultured E18 macrophage-mediated axonal dieback. screening platform using cultured E18 Collectively these data provide compelling hippocampal neurons was used to examine the Collectively these data provide compelling hippocampal neurons was used to examine the Collectively these data provide compelling hippocampal neurons was used to examine the evidence that activation of macrophage TLR2 effects of 5-HT and neuropeptides. Assay plates evidence that activation of macrophage TLR2 effects of 5-HT and neuropeptides. Assay plates evidence that activation of macrophage TLR2 effects of 5-HT and neuropeptides. Assay plates can promote axonal regeneration without were treated with 3 or 30 µM montirelin (TRH can promote axonal regeneration without were treated with 3 or 30 µM montirelin (TRH can promote axonal regeneration without were treated with 3 or 30 µM montirelin (TRH simultaneously eliciting neurotoxic effector analogue), SP or Gal, or 1, 5 or 10 µM simultaneously eliciting neurotoxic effector analogue), SP or Gal, or 1, 5 or 10 µM simultaneously eliciting neurotoxic effector analogue), SP or Gal, or 1, 5 or 10 µM functions. pimozide, alone or in combination with 1 or 10 functions. pimozide, alone or in combination with 1 or 10 functions. pimozide, alone or in combination with 1 or 10 Supported by The Craig H. Neilsen Foundation µM 5-HT for 48 hours. Quantified images Supported by The Craig H. Neilsen Foundation µM 5-HT for 48 hours. Quantified images Supported by The Craig H. Neilsen Foundation µM 5-HT for 48 hours. Quantified images (JCG), American Academy of Neurology showed maximum inhibition of neurite (JCG), American Academy of Neurology showed maximum inhibition of neurite (JCG), American Academy of Neurology showed maximum inhibition of neurite (KAB), NINDS NS037846 (PGP) and The Ray branching in response to 10 µM pimozide. (KAB), NINDS NS037846 (PGP) and The Ray branching in response to 10 µM pimozide. (KAB), NINDS NS037846 (PGP) and The Ray branching in response to 10 µM pimozide. W. Poppleton Endowment (PGP). Intact neurites showed a concentration- W. Poppleton Endowment (PGP). Intact neurites showed a concentration- W. Poppleton Endowment (PGP). Intact neurites showed a concentration- dependent increase in branching in response to dependent increase in branching in response to dependent increase in branching in response to P-83 Reparative Effects Of Raphe-Spinal all of the peptides; some increases in neurite P-83 Reparative Effects Of Raphe-Spinal all of the peptides; some increases in neurite P-83 Reparative Effects Of Raphe-Spinal all of the peptides; some increases in neurite Activity Mediated By 5-Ht7 Receptors, Camp length were also noted. We conclude that 5-HT Activity Mediated By 5-Ht7 Receptors, Camp length were also noted. We conclude that 5-HT Activity Mediated By 5-Ht7 Receptors, Camp length were also noted. We conclude that 5-HT Signalling Cascade, And Co-Released enhances neurotrophic signaling pathways in Signalling Cascade, And Co-Released enhances neurotrophic signaling pathways in Signalling Cascade, And Co-Released enhances neurotrophic signaling pathways in Neuropeptides injured tissue, which can be accentuated by Neuropeptides injured tissue, which can be accentuated by Neuropeptides injured tissue, which can be accentuated by peptides that are often co-released with 5-HT by peptides that are often co-released with 5-HT by peptides that are often co-released with 5-HT by M. M. Carballosa Gonzalez, A. Vitores, A. midbrain and hindbrain raphe nuclei. These M. M. Carballosa Gonzalez, A. Vitores, A. midbrain and hindbrain raphe nuclei. These M. M. Carballosa Gonzalez, A. Vitores, A. midbrain and hindbrain raphe nuclei. These Oliva, I.D. Hentall findings have pharmacotherapeutic implications, Oliva, I.D. Hentall findings have pharmacotherapeutic implications, Oliva, I.D. Hentall findings have pharmacotherapeutic implications,

86 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 86 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 86 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO as well as offer a basis for the restorative effects groups were then assessed for GAG quantity as well as offer a basis for the restorative effects groups were then assessed for GAG quantity as well as offer a basis for the restorative effects groups were then assessed for GAG quantity of raphe stimulation after spinal cord injury and and mRNA expression, and their conditioned of raphe stimulation after spinal cord injury and and mRNA expression, and their conditioned of raphe stimulation after spinal cord injury and and mRNA expression, and their conditioned traumatic brain injury that we report elsewhere. media (CM) used in neurite outgrowth assays of traumatic brain injury that we report elsewhere. media (CM) used in neurite outgrowth assays of traumatic brain injury that we report elsewhere. media (CM) used in neurite outgrowth assays of dorsal root ganglia. There was a significant dorsal root ganglia. There was a significant dorsal root ganglia. There was a significant P-84 Polymer Mediated Delivery Of reduction in XT-I mRNA expression from cells P-84 Polymer Mediated Delivery Of reduction in XT-I mRNA expression from cells P-84 Polymer Mediated Delivery Of reduction in XT-I mRNA expression from cells Xylosyltransferase-I Sirna To Suppress Glial treated with pD-E siRNA polyplexes. This Xylosyltransferase-I Sirna To Suppress Glial treated with pD-E siRNA polyplexes. This Xylosyltransferase-I Sirna To Suppress Glial treated with pD-E siRNA polyplexes. This Scar Glycosaminoglycan Synthesis change in gene expression correlates with Scar Glycosaminoglycan Synthesis change in gene expression correlates with Scar Glycosaminoglycan Synthesis change in gene expression correlates with neurite outgrowth assays, where CM from pD-E neurite outgrowth assays, where CM from pD-E neurite outgrowth assays, where CM from pD-E M. T. Abu-Rub1, M. Naughton1, B. Newland1, N. treated cells resulted in neurite lengths M. T. Abu-Rub1, M. Naughton1, B. Newland1, N. treated cells resulted in neurite lengths M. T. Abu-Rub1, M. Naughton1, B. Newland1, N. treated cells resulted in neurite lengths Madigan2, B. Breen1, S. McMahon3, W. Wang1, significantly higher than CM from untreated Madigan2, B. Breen1, S. McMahon3, W. Wang1, significantly higher than CM from untreated Madigan2, B. Breen1, S. McMahon3, W. Wang1, significantly higher than CM from untreated A. Windebank2, A. Pandit1 cells, and no increase in neurite lengths was A. Windebank2, A. Pandit1 cells, and no increase in neurite lengths was A. Windebank2, A. Pandit1 cells, and no increase in neurite lengths was 1Network of Excellence for Functional observed with the other treatment groups. In 1Network of Excellence for Functional observed with the other treatment groups. In 1Network of Excellence for Functional observed with the other treatment groups. In Biomaterials, National University of Ireland, summary, polymer mediated non-viral delivery Biomaterials, National University of Ireland, summary, polymer mediated non-viral delivery Biomaterials, National University of Ireland, summary, polymer mediated non-viral delivery Galway. Galway, Ireland.; 2Department of of XT-I siRNA to reactive astrocytes provides a Galway. Galway, Ireland.; 2Department of of XT-I siRNA to reactive astrocytes provides a Galway. Galway, Ireland.; 2Department of of XT-I siRNA to reactive astrocytes provides a Neurology. Mayo Clinic College of Medicine. novel approach by which the glial scar Neurology. Mayo Clinic College of Medicine. novel approach by which the glial scar Neurology. Mayo Clinic College of Medicine. novel approach by which the glial scar Rochester, MN, USA.; 3Department of Anatomy, inhibitory pathway can be targeted to facilitate Rochester, MN, USA.; 3Department of Anatomy, inhibitory pathway can be targeted to facilitate Rochester, MN, USA.; 3Department of Anatomy, inhibitory pathway can be targeted to facilitate National University of Ireland, Galway. axonal regrowth. This therapeutic approach is National University of Ireland, Galway. axonal regrowth. This therapeutic approach is National University of Ireland, Galway. axonal regrowth. This therapeutic approach is Galway, Ireland. currently being investigated as part of an Galway, Ireland. currently being investigated as part of an Galway, Ireland. currently being investigated as part of an implantable collagen hydrogel in a rat lateral implantable collagen hydrogel in a rat lateral implantable collagen hydrogel in a rat lateral Glial scar mediated inhibition of axonal spinal cord hemisection model. Glial scar mediated inhibition of axonal spinal cord hemisection model. Glial scar mediated inhibition of axonal spinal cord hemisection model. regrowth following spinal cord injury is regrowth following spinal cord injury is regrowth following spinal cord injury is attributed to increased glycosaminoglycan P-85 Microtubule Stabilization Reduces attributed to increased glycosaminoglycan P-85 Microtubule Stabilization Reduces attributed to increased glycosaminoglycan P-85 Microtubule Stabilization Reduces (GAG) chain production by reactive astrocytes, Scarring And Causes Axon Regeneration (GAG) chain production by reactive astrocytes, Scarring And Causes Axon Regeneration (GAG) chain production by reactive astrocytes, Scarring And Causes Axon Regeneration driven partially by the enzyme After Spinal Cord Injury driven partially by the enzyme After Spinal Cord Injury driven partially by the enzyme After Spinal Cord Injury xylosyltransferase-I (XT-I). The bacterial xylosyltransferase-I (XT-I). The bacterial xylosyltransferase-I (XT-I). The bacterial enzyme chondroitinase ABC, although effective F. Hellal1, A. Hurtado2, J. Ruschel1, KC. Flynn1, enzyme chondroitinase ABC, although effective F. Hellal1, A. Hurtado2, J. Ruschel1, KC. Flynn1, enzyme chondroitinase ABC, although effective F. Hellal1, A. Hurtado2, J. Ruschel1, KC. Flynn1, in alleviating scar-mediated inhibition by CJ. Laskowski1, M. Umlauf1, LC. Kapitein3,4, D. in alleviating scar-mediated inhibition by CJ. Laskowski1, M. Umlauf1, LC. Kapitein3,4, D. in alleviating scar-mediated inhibition by CJ. Laskowski1, M. Umlauf1, LC. Kapitein3,4, D. removing GAG-side chains from core proteins, Strikis5, V. Lemmon5, J. Bixby5, CC. removing GAG-side chains from core proteins, Strikis5, V. Lemmon5, J. Bixby5, CC. removing GAG-side chains from core proteins, Strikis5, V. Lemmon5, J. Bixby5, CC. has a short half-life limiting its bioavailability. Hoogenraad3,4, F. Bradke1 has a short half-life limiting its bioavailability. Hoogenraad3,4, F. Bradke1 has a short half-life limiting its bioavailability. Hoogenraad3,4, F. Bradke1 The overall objective of this study is to provide 1 Deutsches Zentrum für The overall objective of this study is to provide 1 Deutsches Zentrum für The overall objective of this study is to provide 1 Deutsches Zentrum für sustained knockdown of XT-I using small Neurodegenerative Erkrankungen (DZNE), sustained knockdown of XT-I using small Neurodegenerative Erkrankungen (DZNE), sustained knockdown of XT-I using small Neurodegenerative Erkrankungen (DZNE), interfering RNA (siRNA) and a non-viral Axon Growth and Regeneration, Ludwig- interfering RNA (siRNA) and a non-viral Axon Growth and Regeneration, Ludwig- interfering RNA (siRNA) and a non-viral Axon Growth and Regeneration, Ludwig- delivery vehicle comprised of hyperbranched Erhard-Allee 2, 53175 Bonn, Germany; 2 delivery vehicle comprised of hyperbranched Erhard-Allee 2, 53175 Bonn, Germany; 2 delivery vehicle comprised of hyperbranched Erhard-Allee 2, 53175 Bonn, Germany; 2 copolymer (pD-E). The specific objectives are International Center for Spinal Cord Injury, copolymer (pD-E). The specific objectives are International Center for Spinal Cord Injury, copolymer (pD-E). The specific objectives are International Center for Spinal Cord Injury, to: (1) demonstrate efficient siRNA delivery Hugo W. Moser Research Institute at Kennedy to: (1) demonstrate efficient siRNA delivery Hugo W. Moser Research Institute at Kennedy to: (1) demonstrate efficient siRNA delivery Hugo W. Moser Research Institute at Kennedy into reactive astrocytes using pD-E, and Krieger, Department of Neurology, Johns into reactive astrocytes using pD-E, and Krieger, Department of Neurology, Johns into reactive astrocytes using pD-E, and Krieger, Department of Neurology, Johns subsequent knockdown of XT-I, (2) compare Hopkins University, 707 N Broadway, Suite subsequent knockdown of XT-I, (2) compare Hopkins University, 707 N Broadway, Suite subsequent knockdown of XT-I, (2) compare Hopkins University, 707 N Broadway, Suite this effect to other commercially available 523, Baltimore MD, 21205, USA; 3 Department this effect to other commercially available 523, Baltimore MD, 21205, USA; 3 Department this effect to other commercially available 523, Baltimore MD, 21205, USA; 3 Department delivery vehicles, and to (3) test whether this of Neuroscience, Erasmus Medical Center, P.O. delivery vehicles, and to (3) test whether this of Neuroscience, Erasmus Medical Center, P.O. delivery vehicles, and to (3) test whether this of Neuroscience, Erasmus Medical Center, P.O. knockdown reverses the neurite inhibitory Box 2040, 3000 CA Rotterdam, The knockdown reverses the neurite inhibitory Box 2040, 3000 CA Rotterdam, The knockdown reverses the neurite inhibitory Box 2040, 3000 CA Rotterdam, The properties of reactive astrocytes. XT-I siRNA Netherlands; 4 Department of Cell Biology, properties of reactive astrocytes. XT-I siRNA Netherlands; 4 Department of Cell Biology, properties of reactive astrocytes. XT-I siRNA Netherlands; 4 Department of Cell Biology, was used naked or complexed with Faculty of Science, Utrecht University, was used naked or complexed with Faculty of Science, Utrecht University, was used naked or complexed with Faculty of Science, Utrecht University, Lipofectamine 2000 or pD-E. siRNA Padualaan 8, 3584 CH Utrecht, The Lipofectamine 2000 or pD-E. siRNA Padualaan 8, 3584 CH Utrecht, The Lipofectamine 2000 or pD-E. siRNA Padualaan 8, 3584 CH Utrecht, The formulations were then incubated with Neu7 Netherlands.;5 The Miami Project to Cure formulations were then incubated with Neu7 Netherlands.;5 The Miami Project to Cure formulations were then incubated with Neu7 Netherlands.;5 The Miami Project to Cure astrocytes, which overexpress GAGs. Paralysis, University of Miami Miller School of astrocytes, which overexpress GAGs. Paralysis, University of Miami Miller School of astrocytes, which overexpress GAGs. Paralysis, University of Miami Miller School of Astrocytes from the different siRNA treatment Astrocytes from the different siRNA treatment Astrocytes from the different siRNA treatment

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 87 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 87 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 87 ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO

Medicine, 1095 NW 14th Terrace, Miami FL neurons, the growth cone, as they come into first Medicine, 1095 NW 14th Terrace, Miami FL neurons, the growth cone, as they come into first 33136, USA contact with CSPGs in vitro, thus modeling 33136, USA contact with CSPGs in vitro, thus modeling primary interactions with the glial scar. Using primary interactions with the glial scar. Using Hypertrophic scarring and poor intrinsic analyses of time-lapse video images, growth Hypertrophic scarring and poor intrinsic analyses of time-lapse video images, growth axon growth capacity constitute major obstacles cone properties such as morphology, filopodial axon growth capacity constitute major obstacles cone properties such as morphology, filopodial for spinal cord repair. These processes are length and number, approach velocity (to for spinal cord repair. These processes are length and number, approach velocity (to tightly regulated by microtubule dynamics. substratum adsorbed CSPGs), and approach tightly regulated by microtubule dynamics. substratum adsorbed CSPGs), and approach Here, moderate microtubule stabilization angle were compared before and after first Here, moderate microtubule stabilization angle were compared before and after first decreased scar formation after spinal cord injury contact with CSPGs. Using this methodology, decreased scar formation after spinal cord injury contact with CSPGs. Using this methodology, in rodents through various cellular mechanisms, we report that growth cone velocity was in rodents through various cellular mechanisms, we report that growth cone velocity was including dampening of transforming growth significantly reduced following first contact by a including dampening of transforming growth significantly reduced following first contact by a factor–β signaling. It prevented accumulation of single filopodia. We recently reported that factor–β signaling. It prevented accumulation of single filopodia. We recently reported that chondroitin sulfate proteoglycans and rendered single filopodial contact with CSPGs resulted in chondroitin sulfate proteoglycans and rendered single filopodial contact with CSPGs resulted in the lesion site permissive for axon regeneration regulation of growth cone area as well, and the the lesion site permissive for axon regeneration regulation of growth cone area as well, and the of growth-competent sensory neurons. two characteristics may be interrelated. of growth-competent sensory neurons. two characteristics may be interrelated. Microtubule stabilization also promoted growth Collectively, these data are the first Microtubule stabilization also promoted growth Collectively, these data are the first of central nervous system axons of the Raphe- demonstrations of significant behavioral of central nervous system axons of the Raphe- demonstrations of significant behavioral spinal tract and led to functional improvement. changes in growth cone behavior resulting from spinal tract and led to functional improvement. changes in growth cone behavior resulting from Thus, microtubule stabilization reduces fibrotic a single filopodial contact with CSPGs. This Thus, microtubule stabilization reduces fibrotic a single filopodial contact with CSPGs. This scarring and enhances the capacity of axons to intriguing result represents a potential scarring and enhances the capacity of axons to intriguing result represents a potential grow. therapeutic target for regeneration and recovery grow. therapeutic target for regeneration and recovery of function following SCI. [Support provided by of function following SCI. [Support provided by P-86 Single Filopodial Contact With NIH/NINDS (NS053470); the Kentucky Spinal P-86 Single Filopodial Contact With NIH/NINDS (NS053470); the Kentucky Spinal Inhibitory Chondroitin Sulfate Proteoglycans Cord and Brain Injury Research Center (#10- Inhibitory Chondroitin Sulfate Proteoglycans Cord and Brain Injury Research Center (#10- Induces Behavioral Changes In Sensory 11A); the Department of Defense (W81XWH- Induces Behavioral Changes In Sensory 11A); the Department of Defense (W81XWH- Neurons In Vitro 10-1-0778; and the UK Office of Undergraduate Neurons In Vitro 10-1-0778; and the UK Office of Undergraduate Research]. Research]. B. Kulengowski, C. M. Calulot, J. A. Beller, T. B. Kulengowski, C. M. Calulot, J. A. Beller, T. M. Hering, and D. M. Snow P-87 Meningeal/Fibrotic Scar Removal In M. Hering, and D. M. Snow P-87 Meningeal/Fibrotic Scar Removal In The University of Kentucky, Spinal Cord Axolotl Spinal Cord Regeneration The University of Kentucky, Spinal Cord Axolotl Spinal Cord Regeneration and Brain Injury Research Center, Lexington, and Brain Injury Research Center, Lexington, KY 40536. D.A. Sarria, H.V. Nguyen, M.W. Egar and KY 40536. D.A. Sarria, H.V. Nguyen, M.W. Egar and E.A.G. Chernoff E.A.G. Chernoff Chondroitin sulfate proteoglycans Indiana University-Purdue University Chondroitin sulfate proteoglycans Indiana University-Purdue University (CSPGs) are up-regulated in response to spinal Indidanapolis. IU Center for Regenerative (CSPGs) are up-regulated in response to spinal Indidanapolis. IU Center for Regenerative cord injury (SCI), and consequently inhibit Biology and Medicine. Indianapolis, IN 46220. cord injury (SCI), and consequently inhibit Biology and Medicine. Indianapolis, IN 46220. axonal regeneration. The majority of CSPGs axonal regeneration. The majority of CSPGs produced after injury stem from reactive In mammalian penetrating spinal cord produced after injury stem from reactive In mammalian penetrating spinal cord astrocytes of the glial scar. Axons attempting to injuries, such as ballistic wounds, functional astrocytes of the glial scar. Axons attempting to injuries, such as ballistic wounds, functional regrow "evaluate" inhibitory molecules and recovery is inhibited by the production of glial regrow "evaluate" inhibitory molecules and recovery is inhibited by the production of glial make "decisions" about whether to continue to scar basal lamina from reactive astrocytes make "decisions" about whether to continue to scar basal lamina from reactive astrocytes advance, stop, or turn. To grow beyond the glial reinforced by production of a fibrotic scar by advance, stop, or turn. To grow beyond the glial reinforced by production of a fibrotic scar by scar and toward appropriate targets, neurons invading reactive meningeal cells. In mammals scar and toward appropriate targets, neurons invading reactive meningeal cells. In mammals must overcome the CSPG-induced inhibitory the meningeal/fibrotic scar is a major obstacle to must overcome the CSPG-induced inhibitory the meningeal/fibrotic scar is a major obstacle to milieu. The current study examined behavioral axonal regrowth. In salamander regeneration milieu. The current study examined behavioral axonal regrowth. In salamander regeneration changes in the leading edge of regenerating there is also a period of robust meningeal changes in the leading edge of regenerating there is also a period of robust meningeal fibrosis that has been largely unmentioned in fibrosis that has been largely unmentioned in

88 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 88 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO ABSTRACTS OF POSTER PRESENTATIONS - SESSION TWO fibrosis that has been largely unmentioned in traditionalfibrosis that amphibian has been regeneration largely unmentioned literature due in School of Medicine, Irvine, CA 92697-4265; traditional amphibian regeneration literature due School of Medicine, Irvine, CA 92697-4265; traditional amphibian regeneration literature due totraditional the transient amphibian nature regenerationof the fibrosis. literature During duethe 4Division of Occupational Therapy, The Ohio to the transient nature of the fibrosis. During the 4Division of Occupational Therapy, The Ohio to the transient nature of the fibrosis. During the regenerationto the transient of naturetransected of the spinal fibrosis. cord Duringin axolotls the State University regeneration of transected spinal cord in axolotls State University regeneration of transected spinal cord in axolotls (theregeneration salamander of transected Ambystoma spinal mexicanumcord in axolotls),the (the salamander Ambystoma mexicanum),the (the salamander Ambystoma mexicanum),the meningeal(the salamander response Ambystoma causes the mexicanum pia mater),the to Brain function has been studied as a meningeal response causes the pia mater to Brain function has been studied as a meningeal response causes the pia mater to thickenmeningeal from response a single cellcauses layer the to apia layer mater of 4 to determinant of clinical status after spinal cord thicken from a single cell layer to a layer of 4 to determinant of clinical status after spinal cord thicken from a single cell layer to a layer of 4 to 5thicken cells andfrom to a invadesingle cellthe lalesionyer to site a layer depositing of 4 to injury (SCI). Influences on the brain are of 5 cells and to invade the lesion site depositing injury (SCI). Influences on the brain are of 5 cells and to invade the lesion site depositing masses5 cells andof fibrillar to invade collagen. the lesion Invading site depositingarachnoid therefore of interest in this context. The current masses of fibrillar collagen. Invading arachnoid therefore of interest in this context. The current masses of fibrillar collagen. Invading arachnoid cellsmasses are of seenfibrillar in collagen.association Invading with amorphous arachnoid study examined how age, time since injury, cells are seen in association with amorphous study examined how age, time since injury, cells are seen in association with amorphous matrixcells are material. seen in Reactive association ependymal with amorphous cells that motor status, and gait velocity are each related matrix material. Reactive ependymal cells that motor status, and gait velocity are each related matrix material. Reactive ependymal cells that reconstructmatrix material. the Reactivespinal cord ependymal grow intocells thatand to brain function after SCI. A total of 20 reconstruct the spinal cord grow into and to brain function after SCI. A total of 20 reconstruct the spinal cord grow into and remodelreconstruct deposited the spinal extracellular cord grow matrix into andby patients who met eligibility criteria for a study remodel deposited extracellular matrix by patients who met eligibility criteria for a study remodel deposited extracellular matrix by producingremodel depositedmatrix metalloproteinases.extracellular matrix Thisby of mental imagery effects on physical therapy producing matrix metalloproteinases. This of mental imagery effects on physical therapy producing matrix metalloproteinases. This differsproducing from matrixa recent metalloproteinases.report in newts. Our This lab after SCI underwent functional MRI (fMRI) differs from a recent report in newts. Our lab after SCI underwent functional MRI (fMRI) differs from a recent report in newts. Our lab hasdiffers hypothesized from a recent that reportremoval in newts.of the Ourfibrotic lab scanning at baseline. The main entry criteria has hypothesized that removal of the fibrotic scanning at baseline. The main entry criteria has hypothesized that removal of the fibrotic scarhas hypothesizedin salamanders that remisoval dependent of the fibroticupon were age >18 years, incomplete SCI (ASIA C or scar in salamanders is dependent upon were age >18 years, incomplete SCI (ASIA C or scar in salamanders is dependent upon meningeal/ependymalscar in salamanders communicationis dependent at uponthe D), able to ambulate >10 meters with one meningeal/ependymal communication at the D), able to ambulate >10 meters with one meningeal/ependymal communication at the levelmeningeal/ependymal of growth factor andcommunication extracellular atmatrix the person assistance or assistive device, and level of growth factor and extracellular matrix person assistance or assistive device, and level of growth factor and extracellular matrix interactionslevel of growth affecting factor th eand behavior extracellular of both matrix types normal leg range of motion. During fMRI (3 interactions affecting the behavior of both types normal leg range of motion. During fMRI (3 interactions affecting the behavior of both types ofinteractions cells. Coculture affecting of th reactivee behavior ependymal of both types and Tesla), subjects alternated rest with 0.3 Hz right of cells. Coculture of reactive ependymal and Tesla), subjects alternated rest with 0.3 Hz right of cells. Coculture of reactive ependymal and meningealof cells. Coculture material causesof reactive re-epithelialization ependymal and of ankle dorsiflexion. Subjects had age 52.6 +/- meningeal material causes re-epithelialization of ankle dorsiflexion. Subjects had age 52.6 +/- meningeal material causes re-epithelialization of themeningeal reactive material ependyma causes re-epithelialization associated with of 12.1 (mean+/-SD), were 85.8+/- 84.0 months the reactive ependyma associated with 12.1 (mean+/-SD), were 85.8+/- 84.0 months the reactive ependyma associated with restorationthe reactive of ependymathe central associatedcanal in vivowith. post injury, neurological levels C1-L2, and were restoration of the central canal in vivo. post injury, neurological levels C1-L2, and were restoration of the central canal in vivo. Determinationrestoration of ofthe thecentral composition canal inof vivothe. 17 ASIA C/3 ASIA D. Higher age correlated Determination of the composition of the 17 ASIA C/3 ASIA D. Higher age correlated Determination of the composition of the salamanderDetermination fibrotic of thescar compositionis being madeof theto significantly with larger activation in left lateral salamander fibrotic scar is being made to significantly with larger activation in left lateral salamander fibrotic scar is being made to providesalamander a fibroticbasis of scar comparison is being withmade theto postcentral gyrus, bilateral anterior cingulate, provide a basis of comparison with the postcentral gyrus, bilateral anterior cingulate, provide a basis of comparison with the mammalianprovide a fibroticbasis ofscar. comparison Electron microscopy, with the and bilateral medial pre-frontal cortex. Longer mammalian fibrotic scar. Electron microscopy, and bilateral medial pre-frontal cortex. Longer mammalian fibrotic scar. Electron microscopy, histochemicalmammalian fibrotic staining scar. and Electron antibody microscopy, staining time since injury correlated significantly with histochemical staining and antibody staining time since injury correlated significantly with histochemical staining and antibody staining havehistochemical been used staining to loca andlize antibodyand characterize staining larger activation in left lateral postcentral have been used to localize and characterize larger activation in left lateral postcentral have been used to localize and characterize componentshave been usedof theto locasalamanderlize and fibrotic characterize scar. gyrus/inferior parietal lobule and left lateral components of the salamander fibrotic scar. gyrus/inferior parietal lobule and left lateral components of the salamander fibrotic scar. Collagencomponents type of I isthe heavily salamander deposited fibrotic in the lesionscar. frontal lobe. ASIA motor score and gait Collagen type I is heavily deposited in the lesion frontal lobe. ASIA motor score and gait Collagen type I is heavily deposited in the lesion site,Collagen in typethe I isventral-lateral heavily deposited areas in theof lesion the velocity did not correlate significantly with any site, in the ventral-lateral areas of the velocity did not correlate significantly with any site, in the ventral-lateral areas of the regeneratingsite, in the spinal ventral-lateral cord, a phenomenon areas of which the features of brain function. Time has significant regenerating spinal cord, a phenomenon which features of brain function. Time has significant regenerating spinal cord, a phenomenon which hasregenerating been undocumentedspinal cord, a phenomenonuntil now. whichThe effects on the brain after SCI, as both increased has been undocumented until now. The effects on the brain after SCI, as both increased has been undocumented until now. The regenerativehas been undocumentedependymal out growthuntil isnow. associated The age and increased time post-stroke were regenerative ependymal outgrowth is associated age and increased time post-stroke were regenerative ependymal outgrowth is associated withregenerative this type ependymal I collagen. outgrowth is associated associated increased activity. The meaning of with this type I collagen. associated increased activity. The meaning of with this type I collagen. with this type I collagen. these activity increases is open to interpretation, these activity increases is open to interpretation, P-88 Age And Time Since Injury Are but signals an increase use of neural resource in P-88 Age And Time Since Injury Are but signals an increase use of neural resource in Associated With Larger Cortical Activation relation to voluntary movement. The location of Associated With Larger Cortical Activation relation to voluntary movement. The location of After Incomplete Spinal Cord Injury these activation increases is of interest, and After Incomplete Spinal Cord Injury these activation increases is of interest, and might indicate altered sensory processing (post- might indicate altered sensory processing (post- S.C. Cramer1,2, S. Kim3, R. Gramer1, S. Page4, central gyrus) and increased error detection S.C. Cramer1,2, S. Kim3, R. Gramer1, S. Page4, central gyrus) and increased error detection K.G. Sharp1 (anterior cingulate). The current results suggest K.G. Sharp1 (anterior cingulate). The current results suggest 1Reeve-Irvine Research Center, determinants of brain function in subjects with 1Reeve-Irvine Research Center, determinants of brain function in subjects with 2Departments of Anatomy & Neurobiology and incomplete SCI, factors that might be important 2Departments of Anatomy & Neurobiology and incomplete SCI, factors that might be important Neurology, 3Dept of Physical Medicine & to developing and perhaps individualizing spinal Neurology, 3Dept of Physical Medicine & to developing and perhaps individualizing spinal Rehabilitation, University of California at Irvine cord rehabilitation interventions. Rehabilitation, University of California at Irvine cord rehabilitation interventions.

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 89 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 89 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 89 AUTHOR INDEX AUTHOR INDEX AUTHOR INDEX

A Bresnahan, J. C. P-11, P-36 A Bresnahan, J. C. P-11, P-36 A Bresnahan, J. C. P-11, P-36 Brock, J. H. O-1, P-36, Brock, J. H. O-1, P-36, Brock, J. H. O-1, P-36, Abu-Rub, M. T. P-4, P-84 P-37 Abu-Rub, M. T. P-4, P-84 P-37 Abu-Rub, M. T. P-4, P-84 P-37 Airriess, C. P-48 Buckley, A. P-55 Airriess, C. P-48 Buckley, A. P-55 Airriess, C. P-48 Buckley, A. P-55 Alilain, W. J. P-28, P-45 Burger, C. P-29, P-32, Alilain, W. J. P-28, P-45 Burger, C. P-29, P-32, Alilain, W. J. P-28, P-45 Burger, C. P-29, P-32, Alothman, S. P-7, P-8, P-33, P-35 Alothman, S. P-7, P-8, P-33, P-35 Alothman, S. P-7, P-8, P-33, P-35 P-9 Butler, L. E. P-66 P-9 Butler, L. E. P-66 P-9 Butler, L. E. P-66 Alto, L. O-1 Buyukozturk, M. M. P-67 Alto, L. O-1 Buyukozturk, M. M. P-67 Alto, L. O-1 Buyukozturk, M. M. P-67 Angelov, D. P-14 Angelov, D. P-14 Angelov, D. P-14 Angelova, S. P-14 C Angelova, S. P-14 C Angelova, S. P-14 C Ankerne, J. P-14 Ankerne, J. P-14 Ankerne, J. P-14 Armstrong, C. P-49 Calkins, D. J. P-54 Armstrong, C. P-49 Calkins, D. J. P-54 Armstrong, C. P-49 Calkins, D. J. P-54 Ashrafi, M. P-14 Calulot, C. M. P-86 Ashrafi, M. P-14 Calulot, C. M. P-86 Ashrafi, M. P-14 Calulot, C. M. P-86 Assinck, P. P-24 Cantoria, M. J. P-58 Assinck, P. P-24 Cantoria, M. J. P-58 Assinck, P. P-24 Cantoria, M. J. P-58 Athauda, G. P-17 Carballosa Gonzalez, M. M. P-23, P-83 Athauda, G. P-17 Carballosa Gonzalez, M. M. P-23, P-83 Athauda, G. P-17 Carballosa Gonzalez, M. M. P-23, P-83 Atkinson, D. A. P-62 Carlstrom, L. P. P-78 Atkinson, D. A. P-62 Carlstrom, L. P. P-78 Atkinson, D. A. P-62 Carlstrom, L. P. P-78 Ayar, A. P-46 Caudle, K. L. P-62 Ayar, A. P-46 Caudle, K. L. P-62 Ayar, A. P-46 Caudle, K. L. P-62 Chang, T. J. P-29, P-32, Chang, T. J. P-29, P-32, Chang, T. J. P-29, P-32, B P-34 B P-34 B P-34 Chao, T. P-2, P-5 Chao, T. P-2, P-5 Chao, T. P-2, P-5 Badurek, S. P-33, P-35 Chen, Q. P-21 Badurek, S. P-33, P-35 Chen, Q. P-21 Badurek, S. P-33, P-35 Chen, Q. P-21 Barkauskas, D. S. P-20 Chernoff, E. A. G. P-87 Barkauskas, D. S. P-20 Chernoff, E. A. G. P-87 Barkauskas, D. S. P-20 Chernoff, E. A. G. P-87 Bassell, G. J. P-76 Chew, D. P-27 Bassell, G. J. P-76 Chew, D. P-27 Bassell, G. J. P-76 Chew, D. P-27 Beattie, M. S. O-1, P-11, Clark, M. P-45 Beattie, M. S. O-1, P-11, Clark, M. P-45 Beattie, M. S. O-1, P-11, Clark, M. P-45 P-36, P-69 Collinger, J. L. O-5 P-36, P-69 Collinger, J. L. O-5 P-36, P-69 Collinger, J. L. O-5 Beckwith, K. A. P-82 Conner, J. M. P-37 Beckwith, K. A. P-82 Conner, J. M. P-37 Beckwith, K. A. P-82 Conner, J. M. P-37 Beller, J. A. P-74, P-86 Conrad, C. P-53 Beller, J. A. P-74, P-86 Conrad, C. P-53 Beller, J. A. P-74, P-86 Conrad, C. P-53 Beltan, S. O-21 Courtine, G. O-1, P-36 Beltan, S. O-21 Courtine, G. O-1, P-36 Beltan, S. O-21 Courtine, G. O-1, P-36 Benavides, F. P-13, P-17 Cragg, J. J. P-12 Benavides, F. P-13, P-17 Cragg, J. J. P-12 Benavides, F. P-13, P-17 Cragg, J. J. P-12 Benton, R. L. P-53 Craggs, M. P-27 Benton, R. L. P-53 Craggs, M. P-27 Benton, R. L. P-53 Craggs, M. P-27 Bergles, D. E. O-12 Crawford, M. A. P-22 Bergles, D. E. O-12 Crawford, M. A. P-22 Bergles, D. E. O-12 Crawford, M. A. P-22 Bingham, D. P-32 Cregg, J. M. P-77 Bingham, D. P-32 Cregg, J. M. P-77 Bingham, D. P-32 Cregg, J. M. P-77 Bixby, J.L. P-16, P-85 Cruz, C. P-47 Bixby, J.L. P-16, P-85 Cruz, C. P-47 Bixby, J.L. P-16, P-85 Cruz, C. P-47 Blackmore, M. G. P-16 Blackmore, M. G. P-16 Blackmore, M. G. P-16 Blesch, A. O-1, P-37 D Blesch, A. O-1, P-37 D Blesch, A. O-1, P-37 D Blurton-Jones, M. O-8 Blurton-Jones, M. O-8 Blurton-Jones, M. O-8 Bolt, B. P-7, P-8, Dai, H. P-57 Bolt, B. P-7, P-8, Dai, H. P-57 Bolt, B. P-7, P-8, Dai, H. P-57 P-9 Dalley, R. A. P-52 P-9 Dalley, R. A. P-52 P-9 Dalley, R. A. P-52 Bonner, J. O-9 Daly, A. P-15 Bonner, J. O-9 Daly, A. P-15 Bonner, J. O-9 Daly, A. P-15 Boretius, S. O-21 Daly, W. P-4 Boretius, S. O-21 Daly, W. P-4 Boretius, S. O-21 Daly, W. P-4 Boyce, V. S. P-59 Damaser, M. S. P-25 Boyce, V. S. P-59 Damaser, M. S. P-25 Boyce, V. S. P-59 Damaser, M. S. P-25 Boyden, E. S. O-22 Davies, J. P-73 Boyden, E. S. O-22 Davies, J. P-73 Boyden, E. S. O-22 Davies, J. P-73 Bradke, F. P-68, P-85 de Leon, R. D. P-58 Bradke, F. P-68, P-85 de Leon, R. D. P-58 Bradke, F. P-68, P-85 de Leon, R. D. P-58 Brandon, B. P-67 Delivopoulos, E. P-27 Brandon, B. P-67 Delivopoulos, E. P-27 Brandon, B. P-67 Delivopoulos, E. P-27 Breen, B. P-4, P-84 DePaul, M. P-25 Breen, B. P-4, P-84 DePaul, M. P-25 Breen, B. P-4, P-84 DePaul, M. P-25 Bregman, B. P-57 Donaldson, N. P-27 Bregman, B. P-57 Donaldson, N. P-27 Bregman, B. P-57 Donaldson, N. P-27

90 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 90 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 90 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION AUTHOR INDEX AUTHOR INDEX AUTHOR INDEX

Donnelly, C. J. P-76 Ghassemi, O. P-79 Donnelly, C. J. P-76 Ghassemi, O. P-79 Donnelly, C. J. P-76 Ghassemi, O. P-79 Duncan, G. J. P-19, P-24 Giger, R. J. O-20 Duncan, G. J. P-19, P-24 Giger, R. J. O-20 Duncan, G. J. P-19, P-24 Giger, R. J. O-20 Dworski, S. P-24 Gill, M. E. P-54 Dworski, S. P-24 Gill, M. E. P-54 Dworski, S. P-24 Gill, M. E. P-54 Girard, M. P-60 Girard, M. P-60 Girard, M. P-60 Glattfelder, K. J. P-52 Glattfelder, K. J. P-52 Glattfelder, K. J. P-52 Gonzalez-Rothi, E. J. P-15, P-43 Gonzalez-Rothi, E. J. P-15, P-43 Gonzalez-Rothi, E. J. P-15, P-43 E Goshgarian, H. G. P-46 E Goshgarian, H. G. P-46 E Goshgarian, H. G. P-46 Gottliebb, D. I. P-50 Gottliebb, D. I. P-50 Gottliebb, D. I. P-50

Graham, L. P-37 Graham, L. P-37 Graham, L. P-37 Edgar, J. O-21 Edgar, J. O-21 Edgar, J. O-21 Granger, N. P-27 Granger, N. P-27 Granger, N. P-27 Edgerton, V. R. O-1, P-36 Edgerton, V. R. O-1, P-36 Edgerton, V. R. O-1, P-36 Grant, J. P-46 Grant, J. P-46 Grant, J. P-46 Egar, M. W. P-87 Egar, M. W. P-87 Egar, M. W. P-87 Grau, J. W. P-69 Grau, J. W. P-69 Grau, J. W. P-69 Eisel, L. P-14 Eisel, L. P-14 Eisel, L. P-14 Greger, B. O-3 Greger, B. O-3 Greger, B. O-3 Ekeledo, A. P-75 Ekeledo, A. P-75 Ekeledo, A. P-75 Grossl, G. P-26 Grossl, G. P-26 Grossl, G. P-26 Ertürk, A. P-68 Ertürk, A. P-68 Ertürk, A. P-68 Grothe, C. P-3 Grothe, C. P-3 Grothe, C. P-3 Evans, M. P-49 Evans, M. P-49 Evans, M. P-49 Guada, L. P-13, P-17 Guada, L. P-13, P-17 Guada, L. P-13, P-17 Evans, T. A. P-20 Evans, T. A. P-20 Evans, T. A. P-20 Guandique, C. F. P-11 Guandique, C. F. P-11 Guandique, C. F. P-11

Guest, J. P-13, P-17 Guest, J. P-13, P-17 Guest, J. P-13, P-17 F Gupta, R. P-2, P-5 F Gupta, R. P-2, P-5 F Gupta, R. P-2, P-5

Fawcett, J. P-27 H Fawcett, J. P-27 H Fawcett, J. P-27 H Federico, R. A. P-15 Federico, R. A. P-15 Federico, R. A. P-15

Ferguson, A. R. P-11, P-36, Ferguson, A. R. P-11, P-36, Ferguson, A. R. P-11, P-36, Haastert-Talini, K. P-3 Haastert-Talini, K. P-3 Haastert-Talini, K. P-3 P-69 P-69 P-69 Hahn, P. P-2, P-5 Hahn, P. P-2, P-5 Hahn, P. P-2, P-5 Ferguson, D. P-47 Ferguson, D. P-47 Ferguson, D. P-47 Harness, J. P-47, P-49 Harness, J. P-47, P-49 Harness, J. P-47, P-49 Fiorelli, R. P-56 Fiorelli, R. P-56 Fiorelli, R. P-56 Harrach, R. P-14 Harrach, R. P-14 Harrach, R. P-14 Fischer, I. O-9 Fischer, I. O-9 Fischer, I. O-9 Harris, N. P-72 Harris, N. P-72 Harris, N. P-72 Floyd, C. L. P-60 Floyd, C. L. P-60 Floyd, C. L. P-60 Harvey, A. R. P-10 Harvey, A. R. P-10 Harvey, A. R. P-10 Flynn, K. C. P-85 Flynn, K. C. P-85 Flynn, K. C. P-85 Havton, L. A. O-1, P-36, Havton, L. A. O-1, P-36, Havton, L. A. O-1, P-36, Ford, B. D. P-30 Ford, B. D. P-30 Ford, B. D. P-30 P-37 P-37 P-37 Ford, G. D. P-30 Ford, G. D. P-30 Ford, G. D. P-30 Hawbecker, S. P-36 Hawbecker, S. P-36 Hawbecker, S. P-36 Frahm, J. O-21 Frahm, J. O-21 Frahm, J. O-21 He, Z. P-68 He, Z. P-68 He, Z. P-68 Frame, J. P-47 Frame, J. P-47 Frame, J. P-47 Hellal, F. P-85 Hellal, F. P-85 Hellal, F. P-85 Fredrickson, C. P-48 Fredrickson, C. P-48 Fredrickson, C. P-48 Heller, S. O-13 Heller, S. O-13 Heller, S. O-13 Frump, D. P-2, P-5 Frump, D. P-2, P-5 Frump, D. P-2, P-5 Hellström, M. P-10 Hellström, M. P-10 Hellström, M. P-10 Fuenschilling, U. O-21 Fuenschilling, U. O-21 Fuenschilling, U. O-21 Henley, J. R. P-78 Henley, J. R. P-78 Henley, J. R. P-78 Fuller, D. D. P-15, P-26, Fuller, D. D. P-15, P-26, Fuller, D. D. P-15, P-26, Hentall, I. D. P-23, P-83 Hentall, I. D. P-23, P-83 Hentall, I. D. P-23, P-83 P-42, P-43, P-44 P-42, P-43, P-44 P-42, P-43, P-44 Hering, T. M. P-73, P-74, Hering, T. M. P-73, P-74, Hering, T. M. P-73, P-74,

P-86 P-86 P-86 G Hettwer, T. P-3 G Hettwer, T. P-3 G Hettwer, T. P-3 Hill, C. H. P-6 Hill, C. H. P-6 Hill, C. H. P-6 Gage, F. H. P-59 Hilton, B. J. P-19, P-64 Gage, F. H. P-59 Hilton, B. J. P-19, P-64 Gage, F. H. P-59 Hilton, B. J. P-19, P-64 Gallo, G. P-76 Hines, J. H. P-78 Gallo, G. P-76 Hines, J. H. P-78 Gallo, G. P-76 Hines, J. H. P-78 Gao, M. P-37 Hoath, K. L. P-10 Gao, M. P-37 Hoath, K. L. P-10 Gao, M. P-37 Hoath, K. L. P-10 Gates, A. P-30 Hodgetts, S. I. P-55 Gates, A. P-30 Hodgetts, S. I. P-55 Gates, A. P-30 Hodgetts, S. I. P-55 Geller, H. M. O-19, P-70 Hoh, D. J. P-26 Geller, H. M. O-19, P-70 Hoh, D. J. P-26 Geller, H. M. O-19, P-70 Hoh, D. J. P-26 Gensel, J. C. P-82 Gensel, J. C. P-82 Gensel, J. C. P-82

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 91 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 91 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 91 AUTHOR INDEX AUTHOR INDEX AUTHOR INDEX

Hoogenraad, C. C. P-85 Kubler, A. O-2 Hoogenraad, C. C. P-85 Kubler, A. O-2 Hoogenraad, C. C. P-85 Kubler, A. O-2 Horner, P. J. P-54 Kulengowski, B. P-86 Horner, P. J. P-54 Kulengowski, B. P-86 Horner, P. J. P-54 Kulengowski, B. P-86 Hovda, D. P-72 Kwon, B. K. P-24 Hovda, D. P-72 Kwon, B. K. P-24 Hovda, D. P-72 Kwon, B. K. P-24 Howe, C. L. P-81 Howe, C. L. P-81 Howe, C. L. P-81 Howells, D. W. O-15 L Howells, D. W. O-15 L Howells, D. W. O-15 L Hu, Y. P-10 Hu, Y. P-10 Hu, Y. P-10 Huang, A. Y. P-20 Lacour, S. P-27 Huang, A. Y. P-20 Lacour, S. P-27 Huang, A. Y. P-20 Lacour, S. P-27 Huie, J. R. P-69 Lam, C. K. P-24 Huie, J. R. P-69 Lam, C. K. P-24 Huie, J. R. P-69 Lam, C. K. P-24 Humphries, C. E. P-10 Lam, T. P-32 Humphries, C. E. P-10 Lam, T. P-32 Humphries, C. E. P-10 Lam, T. P-32 Hunter, D. V. P-80 Lammertse, D. P. O-16 Hunter, D. V. P-80 Lammertse, D. P. O-16 Hunter, D. V. P-80 Lammertse, D. P. O-16 Hurtado, A. P-85 Lane, M. A. P-15, P-26, Hurtado, A. P-85 Lane, M. A. P-15, P-26, Hurtado, A. P-85 Lane, M. A. P-15, P-26, Hussey, S. P-44 P-40, P-41, P-42, P-43 Hussey, S. P-44 P-40, P-41, P-42, P-43 Hussey, S. P-44 P-40, P-41, P-42, P-43 Lang, B. T. P-77 Lang, B. T. P-77 Lang, B. T. P-77 I LaPlaca, M. P-30 I LaPlaca, M. P-30 I LaPlaca, M. P-30 Laracy, J. P-57 Laracy, J. P-57 Laracy, J. P-57 Inskip, J. A. P-18 Laskowski, C. J. P-85 Inskip, J. A. P-18 Laskowski, C. J. P-85 Inskip, J. A. P-18 Laskowski, C. J. P-85 Irintchev, A. P-14 Lee, C. C. J. P-31, P-32, Irintchev, A. P-14 Lee, C. C. J. P-31, P-32, Irintchev, A. P-14 Lee, C. C. J. P-31, P-32, P-33, P-35 P-33, P-35 P-33, P-35 J Lee, K. Z. P-42 J Lee, K. Z. P-42 J Lee, K. Z. P-42 Lee, K. H. P-69 Lee, K. H. P-69 Lee, K. H. P-69 Jeffery, N. P-27 Lee, S. M. P-75 Jeffery, N. P-27 Lee, S. M. P-75 Jeffery, N. P-27 Lee, S. M. P-75 Jiang, H.H. P-25 Lee, Y. S. P-25 Jiang, H.H. P-25 Lee, Y. S. P-25 Jiang, H.H. P-25 Lee, Y. S. P-25 Jiang, Y. P-24 Lemmon, V. P. P-16, P-85 Jiang, Y. P-24 Lemmon, V. P. P-16, P-85 Jiang, Y. P-24 Lemmon, V. P. P-16, P-85 Jones, A. R. P-52 Levene, H. P-17 Jones, A. R. P-52 Levene, H. P-17 Jones, A. R. P-52 Levene, H. P-17 Julian, A. T. P-10 Lewandowski, G. P-65 Julian, A. T. P-10 Lewandowski, G. P-65 Julian, A. T. P-10 Lewandowski, G. P-65 Jung, J. P-2, P-5 Li, S. P-77 Jung, J. P-2, P-5 Li, S. P-77 Jung, J. P-2, P-5 Li, S. P-77 Just, I. P-3 Lin, C. Y. P-25, P-61 Just, I. P-3 Lin, C. Y. P-25, P-61 Just, I. P-3 Lin, C. Y. P-25, P-61 Lin, M. P-2 Lin, M. P-2 Lin, M. P-2 K Lin, V. W. P-25 K Lin, V. W. P-25 K Lin, V. W. P-25 Liu, A. W. P-11 Liu, A. W. P-11 Liu, A. W. P-11 Kadoya, K. O-1 Liu, J. P-19, P-24, Kadoya, K. O-1 Liu, J. P-19, P-24, Kadoya, K. O-1 Liu, J. P-19, P-24, Kang, J. P-2 P-29, P-31, P-32, P-33, P-34, P-35 Kang, J. P-2 P-29, P-31, P-32, P-33, P-34, P-35 Kang, J. P-2 P-29, P-31, P-32, P-33, P-34, P-35 Kapitein, L. C. P-85 Liu, W. P-11, P-29, Kapitein, L. C. P-85 Liu, W. P-11, P-29, Kapitein, L. C. P-85 Liu, W. P-11, P-29, Katagiri, Y. O-19, P-70, P-31, P-33, P-35 Katagiri, Y. O-19, P-70, P-31, P-33, P-35 Katagiri, Y. O-19, P-70, P-31, P-33, P-35 P-71 Loftus, J. P-43 P-71 Loftus, J. P-43 P-71 Loftus, J. P-43 Keirstead, H. P-47, P-48, Lopez, C. P-43 Keirstead, H. P-47, P-48, Lopez, C. P-43 Keirstead, H. P-47, P-48, Lopez, C. P-43 P-49, P-51 Lorenzana, A. P-79 P-49, P-51 Lorenzana, A. P-79 P-49, P-51 Lorenzana, A. P-79 Kennedy, T. E. P-52 Lu, P. P-37 Kennedy, T. E. P-52 Lu, P. P-37 Kennedy, T. E. P-52 Lu, P. P-37 Kernie, S. G. P-34 Kernie, S. G. P-34 Kernie, S. G. P-34 Khaing, Z. Z. P-28 M Khaing, Z. Z. P-28 M Khaing, Z. Z. P-28 M Kim, J. P-19 Kim, J. P-19 Kim, J. P-19 Kirchhoff, F. O-21 MacFarlane, P. M. P-38 Kirchhoff, F. O-21 MacFarlane, P. M. P-38 Kirchhoff, F. O-21 MacFarlane, P. M. P-38 Kleitman, N. O-14 Madigan, N. P-84 Kleitman, N. O-14 Madigan, N. P-84 Kleitman, N. O-14 Madigan, N. P-84 Kramer, J. K. P-19 Magnuson, D. S. K. P-62 Kramer, J. K. P-19 Magnuson, D. S. K. P-62 Kramer, J. K. P-19 Magnuson, D. S. K. P-62 Krarup, C. P-1 Mahad, D. O-21 Krarup, C. P-1 Mahad, D. O-21 Krarup, C. P-1 Mahad, D. O-21 Krassioukov, A. V. P-18 Mao, S. P-19 Krassioukov, A. V. P-18 Mao, S. P-19 Krassioukov, A. V. P-18 Mao, S. P-19

92 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 92 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 92 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION AUTHOR INDEX AUTHOR INDEX AUTHOR INDEX

Maragakis, N. J. O-10 O Maragakis, N. J. O-10 O Maragakis, N. J. O-10 O Maris, D. O. P-54 Maris, D. O. P-54 Maris, D. O. P-54 Martin – Carreras, T. P-26 O’Connell, C. P-4 Martin – Carreras, T. P-26 O’Connell, C. P-4 Martin – Carreras, T. P-26 O’Connell, C. P-4 Massa, S. P-32 O’Steen, B. E. P-15, P-40, Massa, S. P-32 O’Steen, B. E. P-15, P-40, Massa, S. P-32 O’Steen, B. E. P-15, P-40, McAtee, M. P-57 P-41, P-42, P-43 McAtee, M. P-57 P-41, P-42, P-43 McAtee, M. P-57 P-41, P-42, P-43 McCaig, C. D. O-7 Okano, H. P-47 McCaig, C. D. O-7 Okano, H. P-47 McCaig, C. D. O-7 Okano, H. P-47 McCreedy, D. A. P-50 Oliva, A. P-83 McCreedy, D. A. P-50 Oliva, A. P-83 McCreedy, D. A. P-50 Oliva, A. P-83 McHale, K. P-37 Ozsoy, O. P-14 McHale, K. P-37 Ozsoy, O. P-14 McHale, K. P-37 Ozsoy, O. P-14 McMahon, S. P-27, P-84 Ozsoy, U. P-14 McMahon, S. P-27, P-84 Ozsoy, U. P-14 McMahon, S. P-27, P-84 Ozsoy, U. P-14 Mendell, L. M. P-59 Mendell, L. M. P-59 Mendell, L. M. P-59 Mercier, L. M. P-40, P-42, P Mercier, L. M. P-40, P-42, P Mercier, L. M. P-40, P-42, P P-43 P-43 P-43 Miller, F. D. P-24 Pandit, A. P-4, P-84 Miller, F. D. P-24 Pandit, A. P-4, P-84 Miller, F. D. P-24 Pandit, A. P-4, P-84 Miller, K. E. P-7, P-8, Park, J. P-59 Miller, K. E. P-7, P-8, Park, J. P-59 Miller, K. E. P-7, P-8, Park, J. P-59 P-9 Park, M. P-76 P-9 Park, M. P-76 P-9 Park, M. P-76 Minev, I. P-27 Partida, E. P-58 Minev, I. P-27 Partida, E. P-58 Minev, I. P-27 Partida, E. P-58 Mitchell, G. S. P-38 Peckham, P. H. O-6 Mitchell, G. S. P-38 Peckham, P. H. O-6 Mitchell, G. S. P-38 Peckham, P. H. O-6 Moldovan, M. P-1 Petit, A. P-52 Moldovan, M. P-1 Petit, A. P-52 Moldovan, M. P-1 Petit, A. P-52 Montague, A. P. P-53 Petruska, J. C. P-6 Montague, A. P. P-53 Petruska, J. C. P-6 Montague, A. P. P-53 Petruska, J. C. P-6 Moraes, C. O-21 Plant, G. W. P-55 Moraes, C. O-21 Plant, G. W. P-55 Moraes, C. O-21 Plant, G. W. P-55 Moritz, C. T. O-4 Plemel, J. R. P-19 Moritz, C. T. O-4 Plemel, J. R. P-19 Moritz, C. T. O-4 Plemel, J. R. P-19 Morris, R. P-63 Pollett, M. A. P-10 Morris, R. P-63 Pollett, M. A. P-10 Morris, R. P-63 Pollett, M. A. P-10 Moseanko, R. P-36 Poole, A. P-48, P-51 Moseanko, R. P-36 Poole, A. P-48, P-51 Moseanko, R. P-36 Poole, A. P-48, P-51 Mosse, S. P-27 Popovich, P. G. P-82 Mosse, S. P-27 Popovich, P. G. P-82 Mosse, S. P-27 Popovich, P. G. P-82 Mozaffar, T. P-5 Puchalski, R. B. P-52 Mozaffar, T. P-5 Puchalski, R. B. P-52 Mozaffar, T. P-5 Puchalski, R. B. P-52 Mozer, A. B. P-53 Mozer, A. B. P-53 Mozer, A. B. P-53 R R R N N N Raineteau, O. P-56 Raineteau, O. P-56 Raineteau, O. P-56 Nantwi, K. D. P-39 Ramer, L. M. P-12, P-18 Nantwi, K. D. P-39 Ramer, L. M. P-12, P-18 Nantwi, K. D. P-39 Ramer, L. M. P-12, P-18 Nassiri, N. P-5 Ramer, M. S. P-12, P-22, Nassiri, N. P-5 Ramer, M. S. P-12, P-22, Nassiri, N. P-5 Ramer, M. S. P-12, P-22, Naughton, M. P-84 P-18, P-80 Naughton, M. P-84 P-18, P-80 Naughton, M. P-84 P-18, P-80 Nave, K. A. O-21 Rau, K. K. P-6 Nave, K. A. O-21 Rau, K. K. P-6 Nave, K. A. O-21 Rau, K. K. P-6 Neckel, N. D. P-57 Reier, P. J. P-15, P-40, Neckel, N. D. P-57 Reier, P. J. P-15, P-40, Neckel, N. D. P-57 Reier, P. J. P-15, P-40, Neumann, M. P-31 P-41, P-42, P-43 Neumann, M. P-31 P-41, P-42, P-43 Neumann, M. P-31 P-41, P-42, P-43 Newland, B. P-84 Ribble, A. P-53 Newland, B. P-84 Ribble, A. P-53 Newland, B. P-84 Ribble, A. P-53 Nguyen, H. V. P-87 Rohrbeck, A. P-3 Nguyen, H. V. P-87 Rohrbeck, A. P-3 Nguyen, H. V. P-87 Rohrbeck, A. P-3 Nielsen, F. C. P-1 Rombola, A. P-15 Nielsen, F. C. P-1 Rombola, A. P-15 Nielsen, F. C. P-1 Rombola, A. P-15 Nielson, J. L. P-11, P-36 Rosberg, M. P-1 Nielson, J. L. P-11, P-36 Rosberg, M. P-1 Nielson, J. L. P-11, P-36 Rosberg, M. P-1 Nistor, G. P-47, P-48, Rosenzweig, E. S. O-6, P-36 Nistor, G. P-47, P-48, Rosenzweig, E. S. O-6, P-36 Nistor, G. P-47, P-48, Rosenzweig, E. S. O-6, P-36 P-51 Roskams, A. J. P-52 P-51 Roskams, A. J. P-52 P-51 Roskams, A. J. P-52 Noble-Haeusslein, L. J. O-18, P-31, Rossi, S. P-51 Noble-Haeusslein, L. J. O-18, P-31, Rossi, S. P-51 Noble-Haeusslein, L. J. O-18, P-31, Rossi, S. P-51 P-75 Roy, R. R. P-36 P-75 Roy, R. R. P-36 P-75 Roy, R. R. P-36 Nogueira, M. P-72 Ruschel, J. P-85 Nogueira, M. P-72 Ruschel, J. P-85 Nogueira, M. P-72 Ruschel, J. P-85 Nolta, J. A. O-17 Ryczek, D. F. P-42 Nolta, J. A. O-17 Ryczek, D. F. P-42 Nolta, J. A. O-17 Ryczek, D. F. P-42 Nout, Y. S. P-36 Nout, Y. S. P-36 Nout, Y. S. P-36

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 93 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 93 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 93 AUTHOR INDEX AUTHOR INDEX AUTHOR INDEX

S Sun, C. P-32, P-34, S Sun, C. P-32, P-34, S Sun, C. P-32, P-34, P-35 P-35 P-35 Saab, A. O-21 Sun, H. D. P-34 Saab, A. O-21 Sun, H. D. P-34 Saab, A. O-21 Sun, H. D. P-34 Sakiyama-Elbert, S. E. P-50 Supplie, L. O-21 Sakiyama-Elbert, S. E. P-50 Supplie, L. O-21 Sakiyama-Elbert, S. E. P-50 Supplie, L. O-21 Salazar, K. P-40 Sutton, R. P-72 Salazar, K. P-40 Sutton, R. P-72 Salazar, K. P-40 Sutton, R. P-72 Saloner, R. P-33, P-34 Swanson, R. A. P-32 Saloner, R. P-33, P-34 Swanson, R. A. P-32 Saloner, R. P-33, P-34 Swanson, R. A. P-32 Sanchez, D. E. P-40, P-44 Symes, A. J. P-71 Sanchez, D. E. P-40, P-44 Symes, A. J. P-71 Sanchez, D. E. P-40, P-44 Symes, A. J. P-71 Sanders, A. D. P-52 Sanders, A. D. P-52 Sanders, A. D. P-52 Santamaria, A. P-13, P-17 T Santamaria, A. P-13, P-17 T Santamaria, A. P-13, P-17 T Sarria, D. A. P-87 Sarria, D. A. P-87 Sarria, D. A. P-87 Sauer, B. M. P-81 Terada, J. P-38 Sauer, B. M. P-81 Terada, J. P-38 Sauer, B. M. P-81 Terada, J. P-38 Savage, K. P-60 Tetzlaff, W. P-19, P-24, Savage, K. P-60 Tetzlaff, W. P-19, P-24, Savage, K. P-60 Tetzlaff, W. P-19, P-24, Schempf, G. P-14 P-52, P-64 Schempf, G. P-14 P-52, P-64 Schempf, G. P-14 P-52, P-64 Schmastieg, W. F. P-81 Thompson, L. P-49 Schmastieg, W. F. P-81 Thompson, L. P-49 Schmastieg, W. F. P-81 Thompson, L. P-49 Schmidt, C. E. P-28 Topp, K. P-75 Schmidt, C. E. P-28 Topp, K. P-75 Schmidt, C. E. P-28 Topp, K. P-75 Schönau, E. P-14 Tovar, D. P-13 Schönau, E. P-14 Tovar, D. P-13 Schönau, E. P-14 Tovar, D. P-13 See, P. A. P-58 Trivedi, A. A. P-75 See, P. A. P-58 Trivedi, A. A. P-75 See, P. A. P-58 Trivedi, A. A. P-75 Sellers, D. L. P-54 Tse, H. M. P-60 Sellers, D. L. P-54 Tse, H. M. P-60 Sellers, D. L. P-54 Tse, H. M. P-60 Semler, O. P-14 Tuszynski, M. H. O-1, P-36 Semler, O. P-14 Tuszynski, M. H. O-1, P-36 Semler, O. P-14 Tuszynski, M. H. O-1, P-36 Sharp, J. P-48 Twiss, J. L. P-76 Sharp, J. P-48 Twiss, J. L. P-76 Sharp, J. P-48 Twiss, J. L. P-76 Sharp, K. G. P-66 Tzvetanova, I. O-21 Sharp, K. G. P-66P-66, P-88 Tzvetanova, I. O-21 Sharp, K. G. P-66, P-88 Tzvetanova, I. O-21 Shi, J. P-32 Shi, J. P-32 Shi, J. P-32 Shields, C. P-16 U Shields, C. P-16 U Shields, C. P-16 U Shine, H. D. P-21 Shine, H. D. P-21 Shine, H. D. P-21 Shum-Siu, A. P-62 Umlauf, M. P-85 Shum-Siu, A. P-62 Umlauf, M. P-85 Shum-Siu, A. P-62 Umlauf, M. P-85 Siegenthaler, M. P-48, P-51 Siegenthaler, M. P-48, P-51 Siegenthaler, M. P-48, P-51 Silver, J. P-20, P-25, V Silver, J. P-20, P-25, V Silver, J. P-20, P-25, V P-28, P-45, P-61, P-77 P-28, P-45, P-61, P-77 P-28, P-45, P-61, P-77 Silverman, C. R. P-50 van Stolk, A. P. P-12, P-18 Silverman, C. R. P-50 van Stolk, A. P. P-12, P-18 Silverman, C. R. P-50 van Stolk, A. P. P-12, P-18 Simmons, P. J. P-55 Vandenborne, K. V. P-15 Simmons, P. J. P-55 Vandenborne, K. V. P-15 Simmons, P. J. P-55 Vandenborne, K. V. P-15 Singh, H. P-58 Verley, D. P-72 Singh, H. P-58 Verley, D. P-72 Singh, H. P-58 Verley, D. P-72 Singh, L. P. P-39 Vikeså, J. P-1 Singh, L. P. P-39 Vikeså, J. P-1 Singh, L. P. P-39 Vikeså, J. P-1 Snow, D. M. P-73, P-86 Vinit, S. P-38 Snow, D. M. P-73, P-86 Vinit, S. P-38 Snow, D. M. P-73, P-86 Vinit, S. P-38 Solano, J. P-17 Vitores, A. P-23, P-83 Solano, J. P-17 Vitores, A. P-23, P-83 Solano, J. P-17 Vitores, A. P-23, P-83 Soltesz, I. P-49 Soltesz, I. P-49 Soltesz, I. P-49 Soper, C. P-57 W Soper, C. P-57 W Soper, C. P-57 W Sparling, J. S. P-24 Sparling, J. S. P-24 Sparling, J. S. P-24

Spillane, M. P-76 Spillane, M. P-76 Spillane, M. P-76 Wang, H. O-19 Wang, H. O-19 Wang, H. O-19 Spruance, V. M. P-41 Spruance, V. M. P-41 Spruance, V. M. P-41 Wang, W. P-84 Wang, W. P-84 Wang, W. P-84 Stahl, K. P-47 Stahl, K. P-47 Stahl, K. P-47 Wang, Y. P-35, P-37 Wang, Y. P-35, P-37 Wang, Y. P-35, P-37 Steeves, J. D. P-18 Steeves, J. D. P-18 Steeves, J. D. P-18 Wang, Y. L. P-77 Wang, Y. L. P-77 Wang, Y. L. P-77 Stein, G. P-14 Stein, G. P-14 Stein, G. P-14 Wang, Z. P-16 Wang, Z. P-16 Wang, Z. P-16 Steinberg, G. K. O-11 Steinberg, G. K. O-11 Steinberg, G. K. O-11 Weber, J. L. P-36 Weber, J. L. P-36 Weber, J. L. P-36 Strand, S. C. P-36 Strand, S. C. P-36 Strand, S. C. P-36 Wedemeyer, M. P-47 Wedemeyer, M. P-47 Wedemeyer, M. P-47 Strikis, D. P-85 Strikis, D. P-85 Strikis, D. P-85 Wellmann, K. P-14 Wellmann, K. P-14 Wellmann, K. P-14 Stuck, E. D. P-69 Stuck, E. D. P-69 Stuck, E. D. P-69 Werb, Z. P-75 Werb, Z. P-75 Werb, Z. P-75

94 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 94 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 94 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION AUTHOR INDEX AUTHOR INDEX AUTHOR INDEX

White, T. E. P-30 White, T. E. P-30 White, T. E. P-30 Willenberg, R. P-68 Willenberg, R. P-68 Willenberg, R. P-68 Willis, D. E. P-76 Willis, D. E. P-76 Willis, D. E. P-76 Windebank, A. P-4, P-84 Windebank, A. P-4, P-84 Windebank, A. P-4, P-84 Wirth, F. P-14 Wirth, F. P-14 Wirth, F. P-14 Wu, D. P-37 Wu, D. P-37 Wu, D. P-37 Wu, D. L. P-24 Wu, D. L. P-24 Wu, D. L. P-24 Wu, S. P-31, P-32, Wu, S. P-31, P-32, Wu, S. P-31, P-32, P-34, P-35 P-34, P-35 P-34, P-35 Wyatt, T. J. P-51 Wyatt, T. J. P-51 Wyatt, T. J. P-51

X X X

Xu, M. P-76 Xu, M. P-76 Xu, M. P-76

Y Y Y

Yamanaka, S. P-47 Yamanaka, S. P-47 Yamanaka, S. P-47 Yao, L. P-4 Yao, L. P-4 Yao, L. P-4 Yi, J. O-19, P-70, Yi, J. O-19, P-70, Yi, J. O-19, P-70, P-71 P-71 P-71 Yoo, S. P-76 Yoo, S. P-76 Yoo, S. P-76 Yu, P. O-19, P-70 Yu, P. O-19, P-70 Yu, P. O-19, P-70

Z Z Z

Zamanskaya, R. P-29, P-31 Zamanskaya, R. P-29, P-31 Zamanskaya, R. P-29, P-31 Zeugolis, D. P-4 Zeugolis, D. P-4 Zeugolis, D. P-4 Zhang, H. P-75 Zhang, H. P-75 Zhang, H. P-75 Zhang, Z. P-7, P-8, Zhang, Z. P-7, P-8, Zhang, Z. P-7, P-8, P-9 P-9 P-9 Zheng, B. P-37, P-79 Zheng, B. P-37, P-79 Zheng, B. P-37, P-79 Zheng, P. P-16 Zheng, P. P-16 Zheng, P. P-16 Zhong, H. P-36 Zhong, H. P-36 Zhong, H. P-36 Zhu, L. P-27 Zhu, L. P-27 Zhu, L. P-27 Zimmer, M. B. P-46 Zimmer, M. B. P-46 Zimmer, M. B. P-46

FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 95 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 95 FOURTEENTH INTERNATIONAL SYMPOSIUM ON NEURAL REGENERATION 95