13Th World Congress of Biological Psychiatry FINAL PROGRAMME
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The Role of the Serotonergic System and the Effects of Antidepressants During Brain Development Examined Using in Vivo Pet Imaging and in Vitro Receptor Binding
From THE DEPARTMENT OF CLINICAL NEUROSCIENCE Karolinska Institutet, Stockholm, Sweden THE ROLE OF THE SEROTONERGIC SYSTEM AND THE EFFECTS OF ANTIDEPRESSANTS DURING BRAIN DEVELOPMENT EXAMINED USING IN VIVO PET IMAGING AND IN VITRO RECEPTOR BINDING Stal Saurav Shrestha Stockholm 2014 Cover Illustration: Voxel-wise analysis of the whole monkey brain using the PET radioligand, [11C]DASB showing persistent serotonin transporter upregulation even after more than 1.5 years of fluoxetine discontinuation. All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by Universitetsservice-AB © Stal Saurav Shrestha, 2014 ISBN 978-91-7549-522-4 Serotonergic System and Antidepressants During Brain Development To my family Amaze yourself ! Stal Saurav Shrestha, 2014 The Department of Clinical Neuroscience The role of the serotonergic system and the effects of antidepressants during brain development examined using in vivo PET imaging and in vitro receptor binding AKADEMISK AVHANDLING som för avläggande av medicine doktorsexamen vid Karolinska Institutet offentligen försvaras i CMM föreläsningssalen L8:00, Karolinska Universitetssjukhuset, Solna THESIS FOR DOCTORAL DEGREE (PhD) Stal Saurav Shrestha Date: March 31, 2014 (Monday); Time: 10 AM Venue: Center for Molecular Medicine Lecture Hall Floor 1, Karolinska Hospital, Solna Principal Supervisor: Opponent: Robert B. Innis, MD, PhD Klaus-Peter Lesch, MD, PhD National Institutes of Health University of Würzburg Department of NIMH Department -
Human Surrogate Models of Central Sensitization
Human surrogate models of central sensitization: a critical review and practical guide Charles Quesada, Anna Kostenko, Idy Ho, Caterina Leone, Zahra Nochi, Alexandre Stouffs, Matthias Wittayer, Ombretta Caspani, Nanna Brix Finnerup, André Mouraux, et al. To cite this version: Charles Quesada, Anna Kostenko, Idy Ho, Caterina Leone, Zahra Nochi, et al.. Human surrogate models of central sensitization: a critical review and practical guide. European Journal of Pain, Wiley, In press, 10.1002/ejp.1768. hal-03196193 HAL Id: hal-03196193 https://hal.archives-ouvertes.fr/hal-03196193 Submitted on 12 Apr 2021 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Human surrogate models of central sensitization: a critical review and practical guide Charles Quesada1,2, Anna Kostenko3, Idy Ho4, Caterina Leone5, Zahra Nochi6, Alexandre Stouffs7, Matthias Wittayer3, Ombretta Caspani3, Nanna Brix Finnerup6, André Mouraux7, Gisèle Pickering8, Irene Tracey4, Andrea Truini5, Rolf-Detlef Treede3, Luis Garcia-Larrea1,2* 1) NeuroPain lab, Lyon Centre for Neuroscience (Inserm -
WO 2013/169741 Al 14 November 2013 (14.11.2013) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2013/169741 Al 14 November 2013 (14.11.2013) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 31/401 (2006.01) A61P 9/12 (2006.01) kind of national protection available): AE, AG, AL, AM, A61K 31/405 (2006.01) A61P 25/00 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, A61K 31/7048 (2006.01) BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (21) International Application Number: HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, PCT/US20 13/039904 KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, (22) International Filing Date: ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, 7 May 2013 (07.05.2013) NO, NZ, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, (25) Filing Language: English TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, (26) Publication Language: English ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/644,134 8 May 2012 (08.05.2012) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, (72) Inventors; and UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, (71) Applicants : STEIN, Emily A. -
The Regulation of Lunatic Fringe During Somitogenesis
THE REGULATION OF LUNATIC FRINGE DURING SOMITOGENESIS DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Emily T. Shifley ***** The Ohio State University 2009 Dissertation Committee: Approved by Professor Susan Cole, Advisor Professor Christine Beattie _________________________________ Professor Mark Seeger Advisor Graduate Program in Molecular Genetics Professor Michael Weinstein ABSTRACT Somitogenesis is the morphological hallmark of vertebrate segmentation. Somites bud from the presomitic mesoderm (PSM) in a sequential, periodic fashion and give rise to the rib cage, vertebrae, and dermis and muscles of the back. The regulation of somitogenesis is complex. In the posterior region of the PSM, a segmentation clock operates to organize cohorts of cells into presomites, while in the anterior region of the PSM the presomites are patterned into rostral and caudal compartments (R/C patterning). Both of these stages of somitogenesis are controlled, at least in part, by the Notch pathway and Lunatic fringe (Lfng), a glycosyltransferase that modifies the Notch receptor. To dissect the roles played by Lfng during somitogenesis, we created a novel allele that lacks cyclic Lfng expression within the segmentation clock, but that maintains expression during R/C somite patterning (Lfng∆FCE1). Lfng∆FCE1/∆FCE1 mice have severe defects in their anterior vertebrae and rib cages, but relatively normal sacral and tail vertebrae, unlike Lfng knockouts. Segmentation clock function is differentially affected by the ∆FCE1 deletion; during anterior somitogenesis the expression patterns of many clock genes are disrupted, while during posterior somitogenesis, certain clock components have recovered. R/C patterning occurs relatively normally in Lfng∆FCE1/∆FCE1 embryos, likely contributing to the partial phenotype rescue, and confirming that Lfng ii plays separate roles in the two regions of the PSM. -
Trkb Receptor Signalling: Implications in Neurodegenerative, Psychiatric and Proliferative Disorders
Int. J. Mol. Sci. 2013, 14, 10122-10142; doi:10.3390/ijms140510122 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Review TrkB Receptor Signalling: Implications in Neurodegenerative, Psychiatric and Proliferative Disorders Vivek K. Gupta 1,*, Yuyi You 1, Veer Bala Gupta 2, Alexander Klistorner 1,3 and Stuart L. Graham 1,3 1 Australian School of Advanced Medicine, Macquarie University, F10A, 2 Technology Place, North Ryde, Sydney, NSW 2109, Australia; E-Mails: [email protected] (Y.Y.); [email protected] (A.K.); [email protected] (S.L.G.) 2 Centre of Excellence for Alzheimer’s Disease Research & Care, School of Medical Sciences, Edith Cowan University, Joondalup, WA 6027, Australia; E-Mail: [email protected] 3 Save Sight Institute, Sydney University, Sydney, NSW 2000, Australia * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +61-2-98-123-537; Fax: +61-2-98-123-600. Received: 27 March 2013; in revised form: 27 April 2013 / Accepted: 28 April 2013 / Published: 13 May 2013 Abstract: The Trk family of receptors play a wide variety of roles in physiological and disease processes in both neuronal and non-neuronal tissues. Amongst these the TrkB receptor in particular has attracted major attention due to its critical role in signalling for brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and neurotrophin-4 (NT4). TrkB signalling is indispensable for the survival, development and synaptic plasticity of several subtypes of neurons in the nervous system. Substantial evidence has emerged over the last decade about the involvement of aberrant TrkB signalling and its compromise in various neuropsychiatric and degenerative conditions. -
Caspase-8, Receptor-Interacting Protein Kinase 1 (RIPK1), and RIPK3 Regulate Retinoic Acid-Induced Cell Differentiation and Necroptosis
Cell Death & Differentiation (2020) 27:1539–1553 https://doi.org/10.1038/s41418-019-0434-2 ARTICLE Caspase-8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3 regulate retinoic acid-induced cell differentiation and necroptosis 1,2 1,3 4 3 1,2,4 Masataka Someda ● Shunsuke Kuroki ● Hitoshi Miyachi ● Makoto Tachibana ● Shin Yonehara Received: 1 July 2019 / Revised: 4 October 2019 / Accepted: 4 October 2019 / Published online: 28 October 2019 © The Author(s) 2019. This article is published with open access Abstract Among caspase family members, Caspase-8 is unique, with associated critical activities to induce and suppress death receptor-mediated apoptosis and necroptosis, respectively. Caspase-8 inhibits necroptosis by suppressing the function of receptor-interacting protein kinase 1 (RIPK1 or RIP1) and RIPK3 to activate mixed lineage kinase domain-like (MLKL). Disruption of Caspase-8 expression causes embryonic lethality in mice, which is rescued by depletion of either Ripk3 or Mlkl, indicating that the embryonic lethality is caused by activation of necroptosis. Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced 1234567890();,: 1234567890();,: cell differentiation is independent of Mlkl and necrosome formation. RA treatment obviously enhanced the expression of RA-specific target genes having the retinoic acid response element (RARE) in their promoter regions to induce cell differentiation, and induced marked expression of RIPK1, RIPK3, and MLKL to stimulate necroptosis. Caspase-8 knockdown induced RIPK1 and RIPK3 to translocate into the nucleus and to form a complex with RA receptor (RAR), and RAR interacting with RIPK1 and RIPK3 showed much stronger binding activity to RARE than RAR without RIPK1 or RIPK3. -
Annual Report 2004 Neurobiology R Esearch U
Annual Report 2004 Neurobiology Research U nit Dept. Neurology, Neuroscience Centre Rigshospitalet The H ealth Science Faculty Copenhagen U niversity www.nru.dk F ront page: A 3D reconstruction of a hierarchical clustering. The central blue cluster matches well the spatial location of the cerebral venous vasculature. Liptrot et al., 2004. Preface This annual report provides an overview of the scientific activities that took place within the Neurobiology Research U nit (NRU ) in 2004. Two PhD-theses were defended in 2004: Karen H usted Adams defended her thesis on 5- H T 2A receptor binding measurements in a large healthy control group. H er thesis is the first of many theses to follow from NRU within the field of clinical molecular neuroimaging studies. Kristin Scheuer, MD, defended her thesis on patients with H ereditary Spastic Paraplegia (H SP). She studied cerebral affection in SPG4 linked H SP by employing functional and structural neuroimaging in combination with comprehensive neuropsychological testing. In April, Professor Gitte M. Knudsen was appointed a tenure position as professor at the U niversity of Copenhagen and in June, she replaced Olaf B. Paulson as chairman of NRU . This ‘generation change’ had been carefully planned over several years and consequently the transition went quite smoothly. Professor Olaf B. Paulson remains as professor at NRU and as chairman of the Danish Research Centre for Magnetic Resonance at H vidovre U niversity H ospital. At the Neuroreceptor Mapping Meeting (NRM) that took place in Vancouver, Canada, this summer NRU was selected as a host of NRM in 2006. The preparations are already in full progress (for more information see also www.nrm06.org) and we look very much forward to welcome our colleagues to Copenhagen in July 2006. -
Regulation of Myogenesis by Cardiotrophin-1 and Tgfp Signalling
Regulation of Myogenesis by Cardiotrophin-1 and TGFp signalling Tetsuaki Miyake A dissertation submitted to the Faculty of Graduate Studies in partial fulfillment of the requirements for the degree of Doctor of Philosophy Graduate Programme in Biology York University Toronto, Ontario, Canada Jan 2010 Library and Archives Bibliotheque et 1*1 Canada Archives Canada Published Heritage Direction du Branch Patrimoine de I'edition 395 Wellington Street 395, rue Wellington OttawaONK1A0N4 OttawaONK1A0N4 Canada Canada Your file Votre reference ISBN: 978-0-494-64946-6 Our file Notre reference ISBN: 978-0-494-64946-6 NOTICE: AVIS: The author has granted a non L'auteur a accorde une licence non exclusive exclusive license allowing Library and permettant a la Bibliotheque et Archives Archives Canada to reproduce, Canada de reproduire, publier, archiver, publish, archive, preserve, conserve, sauvegarder, conserver, transmettre au public communicate to the public by par telecommunication ou par I'lnternet, preter, telecommunication or on the Internet, distribuer et vendre des theses partout dans le loan, distribute and sell theses monde, a des fins commerciales ou autres, sur worldwide, for commercial or non support microforme, papier, electronique et/ou commercial purposes, in microform, autres formats. paper, electronic and/or any other formats. The author retains copyright L'auteur conserve la propriete du droit d'auteur ownership and moral rights in this et des droits moraux qui protege cette these. Ni thesis. Neither the thesis nor la these ni des extraits substantiels de celle-ci substantial extracts from it may be ne doivent etre imprimes ou autrement printed or otherwise reproduced reproduits sans son autorisation. -
Species-Specific Oscillation Periods of Human and Mouse Segmentation
bioRxiv preprint doi: https://doi.org/10.1101/650648; this version posted May 26, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Species-specific oscillation periods of human and mouse segmentation clocks 2 are due to cell autonomous differences in biochemical reaction parameters 3 4 Mitsuhiro Matsuda1, 2, Hanako Hayashi1, Jordi Garcia-Ojalvo3, Kumiko Yoshioka- 5 Kobayashi4, Ryoichiro Kageyama4, Yoshihiro Yamanaka5, Makoto Ikeya5, Junya 6 Toguchida4, 5, Cantas Alev5, Miki Ebisuya1, 2* 7 8 1RIKEN Center for Biosystems Dynamics Research (RIKEN BDR) 9 2-2-3 Minatojima-minamimachi, Chuo-ku, 650-0047 Kobe, Japan 10 2European Molecular Biology Laboratory (EMBL) Barcelona 11 Dr. Aiguader 88, 08003 Barcelona, Spain 12 3Department of Experimental and Health Sciences, Universitat Pompeu Fabra 13 Dr. Aiguader 88, 08003 Barcelona, Spain 14 4Institute for Frontier Life and Medical Sciences, Kyoto University 15 Shogoin-Kawahara-cho, Sakyo-ku, 606-8507 Kyoto, Japan 16 5Center for iPS Cell Research and Application (CiRA), Kyoto University 17 53 Shogoin-Kawahara-cho, Sakyo-ku, 606-8507 Kyoto, Japan 18 19 20 *Correspondence to M Ebisuya ([email protected]) 21 1 bioRxiv preprint doi: https://doi.org/10.1101/650648; this version posted May 26, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. -
Department of Clinical Physiology, Nuclear Medicine &
Department of Clinical Physiology, Nuclear Medicine & PET Annual Report 2017 PET 1991 Scanditronix 32 MeV, 1991 GE4096 PET Scanner – – 25 1993 NMR Spectrometer years anniversary 1993 PET Advance Scanner June, 21st 1992-2017 2001 PET/CT Scanner 2005 PET/CT Scanner 2005 Cyclotron 2 The most grateful 2007 HRRT Scanner thank you to 2009 Radiochemistry Synthesizer the John and Birthe Meyer Foundation 2011 PET/MR Scanner 2017 PET/CT Scanner Rigshospitalet · University of Copenhagen Contents Preface ......................................................................................................................................2 Mission and objectives ...............................................................................................................4 Organisation and staff 2017.......................................................................................................6 Highlights 2017 .......................................................................................................................10 Medical secretaries ..................................................................................................................12 The KF Section ........................................................................................................................14 Water damages ........................................................................................................................16 Inauguration of new professor .................................................................................................19 -
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fphar-09-01143 October 8, 2018 Time: 15:40 # 1 ORIGINAL RESEARCH published: 10 October 2018 doi: 10.3389/fphar.2018.01143 Burst-Like Subcutaneous Electrical Stimulation Induces BDNF-Mediated, Cyclotraxin B-Sensitive Central Sensitization in Rat Spinal Cord Jeffri Retamal1,2, Andrea Reyes1, Paulina Ramirez1,2, David Bravo1,2, Alejandro Hernandez1, Teresa Pelissier3, Luis Villanueva4 and Luis Constandil1,2* 1 Laboratory of Neurobiology, Department of Biology, Faculty of Chemistry and Biology, University of Santiago de Chile, Santiago, Chile, 2 Center for the Development of Nanoscience and Nanotechnology (CEDENNA), Santiago, Chile, 3 Program of Molecular and Clinical Pharmacology, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile, 4 Centre de Psychiatrie et Neurosciences, INSERM UMR 894, Paris, France Intrathecal administration of brain derived neurotrophic factor (BDNF) induces long- term potentiation (LTP) and generates long-lasting central sensitization in spinal cord thus mimicking chronic pain, but the relevance of these observations to chronic pain mechanisms is uncertain. Since C-fiber activation by a high-frequency subcutaneous electrical stimulation (SES) protocol causes spinal release of BDNF and induces spinal Edited by: cord LTP, we propose that application of such protocol would be a sufficient condition Ramón Sotomayor-Zárate, Universidad de Valparaíso, Chile for generating long-lasting BDNF-mediated central sensitization. Results showed that Reviewed by: application of burst-like SES to rat toes produced (i) rapid induction of hyperalgesia James W. Grau, that lasted for more than 3 weeks, (ii) early increase of C-reflex activity followed by Texas A&M University, United States Claudio Coddou, increased wind-up scores lasting for more than 1 week, and (iii) early increase followed Universidad Católica del Norte, Chile by late decrease in BDNF protein levels and phosphorylated TrkB that lasted for more *Correspondence: than 1 week. -
Mood Disorders in Huntington's Disease
REVIEW ARTICLE published: 23 April 2014 BEHAVIORAL NEUROSCIENCE doi: 10.3389/fnbeh.2014.00135 Mood disorders in Huntington’s disease: from behavior to cellular and molecular mechanisms Patrick Pla 1,2,3,4, Sophie Orvoen 5, Frédéric Saudou 1,2,3, Denis J. David 5 and Sandrine Humbert 1,2,3* 1 Institut Curie, Orsay, France 2 CNRS UMR3306, Orsay, France 3 INSERM U1005, Orsay, France 4 Faculté des Sciences, Université Paris-Sud, Orsay, France 5 EA3544, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, France Edited by: Huntington’s disease (HD) is a neurodegenerative disorder that is best known for its Benjamin Adam Samuels, Columbia effect on motor control. Mood disturbances such as depression, anxiety, and irritability University, USA also have a high prevalence in patients with HD, and often start before the onset Reviewed by: of motor symptoms. Various rodent models of HD recapitulate the anxiety/depressive Catherine Belzung, Université Francois Rabelais, France behavior seen in patients. HD is caused by an expanded polyglutamine stretch in Emmanuel Brouillet, Commissariat à the N-terminal part of a 350 kDa protein called huntingtin (HTT). HTT is ubiquitously l’Energie Atomique and Centre expressed and is implicated in several cellular functions including control of transcription, National de la Recherche vesicular trafficking, ciliogenesis, and mitosis. This review summarizes progress in Scientifique, France efforts to understand the cellular and molecular mechanisms underlying behavioral *Correspondence: Sandrine Humbert, Institut Curie, disorders in patients with HD. Dysfunctional HTT affects cellular pathways that are Bâtiment 110, 91405 Orsay Cedex, involved in mood disorders or in the response to antidepressants, including BDNF/TrkB France and serotonergic signaling.