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Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2019 Nocturnal gamma-hydroxybutyrate reduces cortisol awakening response and morning kyrunenine pathway metabolites in healthy volunteers Dornbierer, Dario A ; Boxler, M ; Voegel, C D ; Stucky, Benjamin ; Steuer, A E ; Binz, T M ; Baumgartner, M R ; Baur, Diego M ; Quednow, B B ; Kraemer, T ; Seifritz, E ; Landolt, Hans-Peter ; Bosch, O G Abstract: Background Gamma-hydroxybutyrate (GHB; or sodium oxybate) is an endogenous GHB- /GABAB receptor agonist. It is approved for the application in narcolepsy and has been proposed for potential treatment of Alzheimer’s and Parkinson’s disease, fibromyalgia, and depression, all of which involve neuro-immunological processes. Tryptophan catabolites (TRYCATs), the cortisol awakening re- sponse (CAR), and brain derived neurotrophic factor (BDNF) have been suggested as peripheral biomark- ers of neuropsychiatric disorders. GHB has been shown to induce a delayed reduction of T helper and natural killer cell counts and alter basal cortisol levels, but GHB’s effects on TRYCATs, CAR and BDNF are unknown. Methods Therefore, TRYCAT and BDNF serum levels as well as CAR and the affec- tive state (Positive and Negative Affect Schedule, PANAS) were measured in the morning after asingle nocturnal dose of GHB (50 mg/kg body weight) in 20 healthy male volunteers in a placebo-controlled, balanced, randomized, double-blind, cross-over design. Results In the morning after nocturnal GHB administration, the TRYCATs indolelactic acid, kynurenine, kynurenic acid, 3-hydroxykynurenine, and quinolinic acid, the 3-hydroxykynurenine to kynurenic acid ratio and the CAR were significantly re- duced (p<0.05-0.001, Benjamini-Hochberg corrected). -
Functional Heterogeneity Within Rat Orbitofrontal Cortex in Reward Learning and Decision Making
The Journal of Neuroscience, November 1, 2017 • 37(44):10529–10540 • 10529 Viewpoints Functional Heterogeneity within Rat Orbitofrontal Cortex in Reward Learning and Decision Making X Alicia Izquierdo Department of Psychology, Brain Research Institute, Integrative Center for Learning and Memory, and Integrative Center for Addictions, Universityof California at Los Angeles, Los Angeles, California 90095 Rat orbitofrontal cortex (OFC) is located in the dorsal bank of the rhinal sulcus, and is divided into the medial orbital area, ventral orbital area, ventrolateral orbital area, lateral orbital area, dorsolateral orbital area, and agranular insular areas. Over the past 20 years, there has been a marked increase in the number of publications focused on the functions of rat OFC. While collectively this extensive body of work has provided great insight into the functions of OFC, leading to theoretical and computational models of its functions, one issue that has emerged relates to what is defined as OFC because targeting of this region can be quite variable between studies of appetitive behavior, evenwithinthesamespecies.AlsoapparentisthatthereisanoversamplingandundersamplingofcertainsubregionsofratOFCforstudy, andthiswillbedemonstratedhere.TheintentoftheViewpointistosummarizestudiesinratOFC,giventhediversityofwhatgroupsrefer to as “OFC,” and to integrate these with the findings of recent anatomical studies. The primary aim is to help discern functions in reward learning and decision-making, clearing the course for future empirical work. Key words: basolateral amygdala; cognitive flexibility; devaluation; OFC; prefrontal cortex; reversal learning Introduction 2014), confidence estimates (Kepecs et al., 2008), imagination Over the past 20 years, there has been a marked increase in the and insight (Takahashi et al., 2013; Lucantonio et al., 2014, 2015), number of publications focused on the functions of the orbito- Bayesian belief (Jang et al., 2015), cognitive map of task space frontal cortex (OFC) (Fig. -
Product Update Price List Winter 2014 / Spring 2015 (£)
Product update Price list winter 2014 / Spring 2015 (£) Say to affordable and trusted life science tools! • Agonists & antagonists • Fluorescent tools • Dyes & stains • Activators & inhibitors • Peptides & proteins • Antibodies hellobio•com Contents G protein coupled receptors 3 Glutamate 3 Group I (mGlu1, mGlu5) receptors 3 Group II (mGlu2, mGlu3) receptors 3 Group I & II receptors 3 Group III (mGlu4, mGlu6, mGlu7, mGlu8) receptors 4 mGlu – non-selective 4 GABAB 4 Adrenoceptors 4 Other receptors 5 Ligand Gated ion channels 5 Ionotropic glutamate receptors 5 NMDA 5 AMPA 6 Kainate 7 Glutamate – non-selective 7 GABAA 7 Voltage-gated ion channels 8 Calcium Channels 8 Potassium Channels 9 Sodium Channels 10 TRP 11 Other Ion channels 12 Transporters 12 GABA 12 Glutamate 12 Other 12 Enzymes 13 Kinase 13 Phosphatase 14 Hydrolase 14 Synthase 14 Other 14 Signaling pathways & processes 15 Proteins 15 Dyes & stains 15 G protein coupled receptors Cat no. Product name Overview Purity Pack sizes and prices Glutamate: Group I (mGlu1, mGlu5) receptors Agonists & activators HB0048 (S)-3-Hydroxyphenylglycine mGlu1 agonist >99% 10mg £112 50mg £447 HB0193 CHPG Sodium salt Water soluble, selective mGlu5 agonist >99% 10mg £59 50mg £237 HB0026 (R,S)-3,5-DHPG Selective mGlu1 / mGlu5 agonist >99% 10mg £70 50mg £282 HB0045 (S)-3,5-DHPG Selective group I mGlu receptor agonist >98% 1mg £42 5mg £83 10mg £124 HB0589 S-Sulfo-L-cysteine sodium salt mGlu1α / mGlu5a agonist 10mg £95 50mg £381 Antagonists HB0049 (S)-4-Carboxyphenylglycine Competitive, selective group 1 -
Ligand-Gated Ion Channels
S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2015/16: Ligand-gated ion channels. British Journal of Pharmacology (2015) 172, 5870–5903 THE CONCISE GUIDE TO PHARMACOLOGY 2015/16: Ligand-gated ion channels Stephen PH Alexander1, John A Peters2, Eamonn Kelly3, Neil Marrion3, Helen E Benson4, Elena Faccenda4, Adam J Pawson4, Joanna L Sharman4, Christopher Southan4, Jamie A Davies4 and CGTP Collaborators L 1 School of Biomedical Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK, N 2Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK, 3School of Physiology and Pharmacology, University of Bristol, Bristol, BS8 1TD, UK, 4Centre for Integrative Physiology, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2015/16 provides concise overviews of the key properties of over 1750 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/ doi/10.1111/bph.13350/full. Ligand-gated ion channels are one of the eight major pharmacological targets into which the Guide is divided, with the others being: ligand-gated ion channels, voltage- gated ion channels, other ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The Concise Guide is published in landscape format in order to facilitate comparison of related targets. -
Functional Comparisons of Three Glutamate Transporter Subtypes Cloned from Human Motor Cortex
The Journal of Neuroscience, September 1994, 14(g): 5559-5569 Functional Comparisons of Three Glutamate Transporter Subtypes Cloned from Human Motor Cortex Jeffrey L. Arriza, Wendy A. Fairman, Jacques I. Wadiche, Geoffrey H. Murdoch, Michael P. Kavanaugh, and Susan G. Amara The Vellum Institute for Advanced Biomedical Research, Oregon Health Sciences University, Portland, Oregon 97201 Reuptake plays an important role in regulating synaptic and peripheral tissues(Christensen, 1990) and in the nervous system extracellular concentrations of glutamate. Three glutamate (Kanner and Schuldiner, 1987; Nicholls and Attwell, 1990). transporters expressed in human motor cortex, termed Transport serves a special function in the brain by mediating EAATl , EAATP, and EAAT3 (for excitatory amino acid trans- the reuptake of glutamate releasedat excitatory synapses.Glu- porter), have been characterized by their molecular cloning tamate can be reaccumulated from the synaptic cleft by the and functional expression. Each EAAT subtype mRNA was presynaptic nerve terminal (Eliasof and Werblin, 1993) or by found in all human brain regions analyzed. The most prom- glial uptake of transmitter diffusing from the cleft (Nicholls and inent regional variation in message content was in cerebel- Attwell, 1990; Schwartz and Tachibana, 1990; Barbour et al., lum where EAATl expression predominated. EAATl and 199 1). The activities of neuronal and glial transporters influence EAAT3 mRNAs were also expressed in various non-nervous the temporal and spatial dynamics of the chemical signal in tissues, whereas expression of EAATS was largely restricted other neurotransmitter systems(Hille, 1992; Bruns et al., 1993; to brain. The kinetic parameters and pharmacological char- Isaacsonet al., 1993), but such effects have not yet been dem- acteristics of transport mediated by each EAAT subtype onstrated at glutamatergic synapses(Hestrin et al., 1990; Sar- were determined in transfected mammalian cells by radio- antis et al., 1993). -
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The Journal of Neuroscience, March 2, 2005 • 25(9):2285–2294 • 2285 Development/Plasticity/Repair Neurosteroid-Induced Plasticity of Immature Synapses via Retrograde Modulation of Presynaptic NMDA Receptors Manuel Mameli, Mario Carta, L. Donald Partridge, and C. Fernando Valenzuela Department of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131 Neurosteroids are produced de novo in neuronal and glial cells, which begin to express steroidogenic enzymes early in development. Studies suggest that neurosteroids may play important roles in neuronal circuit maturation via autocrine and/or paracrine actions. However, the mechanism of action of these agents is not fully understood. We report here that the excitatory neurosteroid pregnenolone sulfate induces a long-lasting strengthening of AMPA receptor-mediated synaptic transmission in rat hippocampal neurons during a restricted developmental period. Using the acute hippocampal slice preparation and patch-clamp electrophysiological techniques, we found that pregnenolone sulfate increases the frequency of AMPA-mediated miniature excitatory postsynaptic currents in CA1 pyrami- dal neurons. This effect could not be observed in slices from rats older than postnatal day 5. The mechanism of action of pregnenolone sulfate involved a short-term increase in the probability of glutamate release, and this effect is likely mediated by presynaptic NMDA receptors containing the NR2D subunit, which is transiently expressed in the hippocampus. The increase in glutamate release triggered a long-term enhancement of AMPA receptor function that requires activation of postsynaptic NMDA receptors containing NR2B sub- units. Importantly, synaptic strengthening could also be triggered by postsynaptic neuron depolarization, and an anti-pregnenolone sulfate antibody scavenger blocked this effect. -
OCD Candidate Gene SLC1A1/EAAT3 Impacts Basal Ganglia-Mediated Activity and Stereotypic Behavior
OCD candidate gene SLC1A1/EAAT3 impacts basal ganglia-mediated activity and stereotypic behavior Isaac D. Zikea, Muhammad O. Chohanb, Jared M. Kopelmanc,d,e, Emily N. Krasnowb, Daniel Flickerf,g,h,i, Katherine M. Nautiyalj,k, Michael Bubserl, Christoph Kellendonkm,n,o,p, Carrie K. Jonesa,l, Gregg Stanwoodq, Kenji Fransis Tanakar, Holly Mooreb, Susanne E. Ahmaric,d,e,1, and Jeremy Veenstra-VanderWeeleb,m,n,1 aDepartment of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232; bNew York State Psychiatric Institute, New York, NY 10032; cDepartment of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15260; dCenter for Neuroscience Program, University of Pittsburgh, Pittsburgh, PA 15260; eCenter for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA 15260; fHoward Hughes Medical Institute, Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114; gCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114; hDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115; iBroad Institute, Cambridge, MA 02142; jDepartment of Psychiatry, Columbia University Medical Center, New York, NY 10032; kDivision of Integrative Neuroscience, New York State Psychiatric Institute, New York, NY 10032; lVanderbilt Center for Neuroscience Drug Discovery, Vanderbilt University Medical Center, Nashville, TN 37232; mDepartment of Psychiatry, Columbia University Medical Center, New York, NY 10032; nSackler Institute for Developmental Psychobiology, Columbia University Medical Center, New York, NY 10032; oDepartment of Anesthesiology, Columbia University Medical Center, New York, NY 10032; pDivision of Molecular Therapeutics, New York State Psychiatric Institute, New York, NY 10032; qDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32304; and rDepartment of Neuropsychiatry, School of Medicine, Keio University, Tokyo 108-8345, Japan Edited by Susan G. -
Neuronal and Glial Mechanisms Underlying BBB Dysfunction-Induced Epileptogenesis
Neuronal and Glial Mechanisms Underlying BBB Dysfunction-Induced Epileptogenesis Thesis submitted in partial fulfillment of the requirements for the degree of “DOCTOR OF PHILOSOPHY” by Yaron David Submitted to the Senate of Ben-Gurion University of the Negev November 2011 Beer-Sheva Neuronal and Glial Mechanisms Underlying BBB Dysfunction-Induced Epileptogenesis Thesis submitted in partial fulfillment of the requirements for the degree of “DOCTOR OF PHILOSOPHY” by Yaron David Submitted to the Senate of Ben-Gurion University of the Negev Approved by the advisor_________ Approved by the Dean of the Kreitman School of Advanced Graduate Studies_______ November 2011 Beer-Sheva This work was carried out under the supervision of Professor Alon Friedman The department of Physiology, Faculty of Health Sciences Ben-Gurion University of the Negev. First and foremost, I would like to thank my mentor, Prof. Alon Friedman, who offered an opportunity to a young student who knew absolutely nothing in the field of neuroscience. Your enthusiasm for the pursuit of knowledge is contagious. I also thank you for being a friend. I would like to thanks all those people I encountered throughout the years: Oren Tomkins who brought me to the lab. Uwe Heinemann who kindly opened the gates of the Institute fur Physiologie, in Berlin for me. Sebastian Ivens, for teaching me electrophysiology and being a good friend. Daniela Kaufer and Luisa P. Flores from UC Berkley, without whom I am sure I wouldn‘t have any molecular studies to present. Ilya Fleidervish, with whom every hour is like a semester of teaching. Maya Ketzef, a good friend which never ceases to help me and others. -
Mitlibraries Email: [email protected] Document Services
Room 14-0551 77 Massachusetts Avenue Cambridge, MA 02139 Ph: 617.253.5668 Fax: 617.253.1690 MITLibraries Email: [email protected] Document Services http://libraries.mit.edu/docs DISCLAIMER OF QUALITY Due to the condition of the original material, there are unavoidable flaws in this reproduction. We have made every effort possible to provide you with the best copy available. If you are dissatisfied with this product and find it unusable, please contact Document Services as soon as possible. Thank you. Some pages in the original document contain pictures, graphics, or text that is illegible. EXCITOTOXIC MECHANISMS IN HUNTINGTON'S DISEASE by MIT LIBRARIES JU N 09 1992 Andrew Freese SCHERING Submitted to the Division of Health Sciences and Technology in partial fulfillment of the requirements for the degree of Doctor of Philosophy at the MASSACHUSETTS INSTITUTE OF TECHNOLOGY November, 1991 Copyright (c) 1991, Massachusetts Institute of Technology Signature of Autthor__ - _ , ,- r,~- ~ ,_r1__ , ,,...C Division of Health Sciences and Technology November, 1991 Certified by G.E. Schneider, Thesis Sponsor J.B. Martin, Thesis Advisor M. DiFiglia, Thesis Advisor A Accepted by by_MASCUET _ _ __ _ Chairman,___ _ _ _____,T MASSACHUSETTS INSTNTE Chairman, Department Committee OF TECHNIOI OGY J N',0 7 1992 LIBRARIES "-.r. _ . ^ 1-. a.1 1f. "This doctoral thesis has been examined by a Committee of the Division of Health Sciences and Technology as follows:" Professor William Thilly Chairman Professor Gerald Schneider Thesis Snsor Professor Joseph Martin ..... _ f .. -- Thesis Advisor J..__ Professor Marian DiFiglia Thesis Advisor - - Professor Helmut Zarbl -C---~----'~ it / Professor Edward Bird U- - - - - I - 1dl I' I I Abstract Acting at the N-methyl-D-aspartate (NMDA) excitatory amino acid receptor, a variety of endogenously synthesized excitotoxic compounds, including glutamate and quinolinic acid (QUIN), may play a role in the pathogenesis of a number of neurodegenerative diseases, including Huntington's Disease. -
Opposing Synaptic Regulation of Amyloid-Β Metabolism by NMDA Receptors in Vivo Deborah K
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2011 Opposing synaptic regulation of amyloid-β metabolism by NMDA receptors in vivo Deborah K. Verges Washington University School of Medicine in St. Louis Jessica L. Restivo Washington University School of Medicine in St. Louis Whitney D. Goebel Washington University in St Louis David M. Holtzman Washington University School of Medicine in St. Louis John R. Cirrito Washington University School of Medicine in St. Louis Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Part of the Medicine and Health Sciences Commons Recommended Citation Verges, Deborah K.; Restivo, Jessica L.; Goebel, Whitney D.; Holtzman, David M.; and Cirrito, John R., ,"Opposing synaptic regulation of amyloid-β metabolism by NMDA receptors in vivo." The ourJ nal of Neuroscience.,. 11328-11337. (2011). https://digitalcommons.wustl.edu/open_access_pubs/371 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. 11328 • The Journal of Neuroscience, August 3, 2011 • 31(31):11328–11337 Neurobiology of Disease Opposing Synaptic Regulation of Amyloid- Metabolism by NMDA Receptors In Vivo Deborah K. Verges,1 Jessica L. Restivo,1 Whitney D. Goebel,1 David M. Holtzman,1,2,3,4 and John R. Cirrito1,3,4 Departments of 1Neurology and 2Developmental Biology, 3Hope Center for Neurological Disorders, and 4Knight Alzheimer’s Disease Research Center, Washington University School of Medicine, St. Louis, Missouri 63110 The concentration of amyloid- (A) within the brain extracellular space is one determinant of whether the peptide will aggregate into toxic species that are important in Alzheimer’s disease (AD) pathogenesis. -
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Pain Perception in Neurodevelopmental Animal Models of Schizophrenia
Physiol. Res. 59: 811-819, 2010 Pain Perception in Neurodevelopmental Animal Models of Schizophrenia M. FRANĚK1, S. VACULÍN1, A. YAMAMOTOVÁ1, F. ŠŤASTNÝ2, V. BUBENÍKOVÁ- VALEŠOVÁ2, R. ROKYTA1 1Charles University in Prague, Third Faculty of Medicine, Department of Normal, Pathological and Clinical Physiology, Prague, Czech Republic, 2Prague Psychiatric Center affiliated with the Charles University in Prague, Prague, Czech Republic Received February 17, 2009 Accepted January 18, 2010 On-line April 20, 2010 Summary Corresponding author Animal models are important for the investigation of mechanisms Miloslav Franek, Charles University in Prague, Third Medical and therapeutic approaches in various human diseases, including Faculty, Department of Normal, Pathological and Clinical schizophrenia. Recently, two neurodevelopmental rat models of Physiology, Ke Karlovu 4, 120 00 Prague 2, Czech Republic. this psychosis were developed based upon the use of subunit Fax: +420 224 916 896. E-mail: [email protected] selective N-methyl-D-aspartate receptor agonists – quinolinic acid (QUIN) and N-acetyl-aspartyl-glutamate (NAAG). The aim of this study was to evaluate pain perception in these models. QUIN or Introduction NAAG was infused into lateral cerebral ventricles neonatally. In the adulthood, the pain perception was examined. The rats with Schizophrenia is a neurodevelopmental disorder neonatal brain lesions did not show any significant differences in which afflicts about 1 % of the human population acute mechanical nociception and in formalin test compared to worldwide. The etiology and pathogenesis of this controls. However, the neonatally lesioned rats exhibited psychosis is complex but involves the interplay of significantly higher pain thresholds in thermal nociception. polygenic influences and environmental risk factors Increased levels of mechanical hyperalgesia, accompanying the operating on brain maturation processes.