Monoaminergic Receptors in the Stomatogastric Nervous System: Characterization and Localization in Panulirus Interruptus
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Non-classical amine recognition evolved in a large clade of olfactory receptors The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Li, Qian, Yaw Tachie-Baffour, Zhikai Liu, Maude W Baldwin, Andrew C Kruse, and Stephen D Liberles. 2015. “Non-classical amine recognition evolved in a large clade of olfactory receptors.” eLife 4 (1): e10441. doi:10.7554/eLife.10441. http://dx.doi.org/10.7554/ eLife.10441. Published Version doi:10.7554/eLife.10441 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:23993622 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA RESEARCH ARTICLE Non-classical amine recognition evolved in a large clade of olfactory receptors Qian Li1, Yaw Tachie-Baffour1, Zhikai Liu1, Maude W Baldwin2, Andrew C Kruse3, Stephen D Liberles1* 1Department of Cell Biology, Harvard Medical School, Boston, United States; 2Department of Organismic and Evolutionary Biology, Museum of Comparative Zoology, Harvard University, Cambridge, United States; 3Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, United States Abstract Biogenic amines are important signaling molecules, and the structural basis for their recognition by G Protein-Coupled Receptors (GPCRs) is well understood. Amines are also potent odors, with some activating olfactory trace amine-associated receptors (TAARs). Here, we report that teleost TAARs evolved a new way to recognize amines in a non-classical orientation. -
Neurotransmitters-Drugs Andbrain Function.Pdf
Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Neurotransmitters, Drugs and Brain Function Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Neurotransmitters, Drugs and Brain Function Edited by R. A. Webster Department of Pharmacology, University College London, UK JOHN WILEY & SONS, LTD Chichester Á New York Á Weinheim Á Brisbane Á Singapore Á Toronto Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Copyright # 2001 by John Wiley & Sons Ltd. Bans Lane, Chichester, West Sussex PO19 1UD, UK National 01243 779777 International ++44) 1243 779777 e-mail +for orders and customer service enquiries): [email protected] Visit our Home Page on: http://www.wiley.co.uk or http://www.wiley.com All Rights Reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, scanning or otherwise, except under the terms of the Copyright, Designs and Patents Act 1988 or under the terms of a licence issued by the Copyright Licensing Agency Ltd, 90 Tottenham Court Road, London W1P0LP,UK, without the permission in writing of the publisher. Other Wiley Editorial Oces John Wiley & Sons, Inc., 605 Third Avenue, New York, NY 10158-0012, USA WILEY-VCH Verlag GmbH, Pappelallee 3, D-69469 Weinheim, Germany John Wiley & Sons Australia, Ltd. -
Differential Regulation of Mecp2 Phosphorylation in the CNS by Dopamine and Serotonin
Neuropsychopharmacology (2012) 37, 321–337 & 2012 American College of Neuropsychopharmacology. All rights reserved 0893-133X/12 www.neuropsychopharmacology.org Differential Regulation of MeCP2 Phosphorylation in the CNS by Dopamine and Serotonin 1 1 2 1,2,3,4 ,1 Ashley N Hutchinson , Jie V Deng , Dipendra K Aryal , William C Wetsel and Anne E West* 1 2 Department of Neurobiology, Duke University Medical Center, Durham, NC, USA; Department of Psychiatry and Behavioral Sciences, Duke 3 University Medical Center, Durham, NC, USA; Mouse Behavioral and Neuroendocrine Analysis Core Facility, Duke University Medical Center, 4 Durham, NC, USA; Department of Cell Biology, Duke University Medical Center, Durham, NC, USA Systemic administration of amphetamine (AMPH) induces phosphorylation of MeCP2 at Ser421 (pMeCP2) in select populations of neurons in the mesolimbocortical brain regions. Because AMPH simultaneously activates multiple monoamine neurotransmitter systems, here we examined the ability of dopamine (DA), serotonin (5-HT), and norepinephrine (NE) to induce pMeCP2. Selective blockade of the DA transporter (DAT) or the 5-HT transporter (SERT), but not the NE transporter (NET), was sufficient to induce pMeCP2 in the CNS. DAT blockade induced pMeCP2 in the prelimbic cortex (PLC) and nucleus accumbens (NAc), whereas SERT blockade induced pMeCP2 only in the NAc. Administration of selective DA and 5-HT receptor agonists was also sufficient to induce pMeCP2; however, the specific combination of DA and 5-HT receptors activated determined the regional- and cell-type specificity of pMeCP2 induction. The D1-class DA receptor agonist SKF81297 induced pMeCP2 widely; however, coadministration of the D2-class agonist quinpirole restricted the induction of pMeCP2 to GABAergic interneurons of the NAc. -
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Anatomical and functional evidence for trace amines as unique modulators of locomotor function in the mammalian spinal cord Elizabeth A. Gozal, Emory University Brannan E. O'Neill, Emory University Michael A. Sawchuk, Emory University Hong Zhu, Emory University Mallika Halder, Emory University Chou Ching-Chieh , Emory University Shawn Hochman, Emory University Journal Title: Frontiers in Neural Circuits Volume: Volume 8 Publisher: Frontiers | 2014-11-07, Pages 134-134 Type of Work: Article | Final Publisher PDF Publisher DOI: 10.3389/fncir.2014.00134 Permanent URL: https://pid.emory.edu/ark:/25593/mr95r Final published version: http://dx.doi.org/10.3389/fncir.2014.00134 Copyright information: © 2014 Gozal, O'Neill, Sawchuk, Zhu, Halder, Chou and Hochman. This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires credit be given to copyright holder and/or author, copyright and license notices be kept intact. Accessed September 27, 2021 11:18 AM EDT ORIGINAL RESEARCH ARTICLE published: 07 November 2014 NEURAL CIRCUITS doi: 10.3389/fncir.2014.00134 Anatomical and functional evidence for trace amines as unique modulators of locomotor function in the mammalian spinal cord Elizabeth A. Gozal , Brannan E. O’Neill , Michael A. Sawchuk , Hong Zhu , Mallika Halder , Ching-Chieh Chou and Shawn Hochman* Physiology Department, Emory University, Atlanta, GA, USA Edited by: The trace amines (TAs), tryptamine, tyramine, and β-phenylethylamine, are synthesized Brian R. -
Strengthening Families Together 3Rd Edition Strengthening Families Together 3Rd Edition
Strengthening Families Together 3rd Edition Strengthening Families Together 3rd Edition Helping Canadians Live with Mental Illness The Schizophrenia Society of Canada is interested in hearing from you. If you find this resource helpful, or if you have any suggestions or questions, please let us know. E-mail messages can be sent to [email protected], or phone 905.415.2007. Production of the original materials for Strengthening Families Together was made possible by an educational grant from AstraZeneca Canada Inc. The Early Intervention adaptation was made possible by a grant from the Crabtree Foundation and Eli Lilly Canada. The views expressed herein do not necessarily reflect those of AstraZeneca Canada Inc., the Crabtree Foundation or Eli Lilly Canada. Copyright © 2008 Schizophrenia Society of Canada Revised and updated 2008 All rights reserved. The use of any part of this publication reproduced, transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, or stored in a retrieval system, without prior written consent of the publisher, is an infringement of the copyright law. Editing: Edna Barker Design: Hansen Design 1 Strengthening Families Together: 3rd Edition Helping Canadians Live with Mental Illness | handout Acknowledgements Production of the original Strengthening Families Together program (SFT) was made possible by a series of grants from AstraZeneca Canada Inc. The hard work of a number of people at the British Columbia Schizophrenia Society, including Ms. Nicole Chovil, Director of Education, and Gary Glacken, Executive Director, was instrumental in developing the original Strengthening Families Together program. This edition, designed to meet the needs of a range of families, including those who are newer to psychotic illness, was made possible by a grant from the Crabtree Foundation and Eli Lilly Canada. -
Receptor Interaction Profiles of 4-Alkoxy-Substituted 2,5-Dimethoxyphenethylamines and Related Amphetamines
ORIGINAL RESEARCH published: 28 November 2019 doi: 10.3389/fphar.2019.01423 Receptor Interaction Profiles of 4-Alkoxy-Substituted 2,5-Dimethoxyphenethylamines and Related Amphetamines Karolina E. Kolaczynska 1, Dino Luethi 1,2, Daniel Trachsel 3, Marius C. Hoener 4 and Matthias E. Liechti 1* 1 Division of Clinical Pharmacology and Toxicology, Department of Biomedicine, University Hospital Basel and University of Basel, Basel, Switzerland, 2 Center for Physiology and Pharmacology, Institute of Pharmacology, Medical University of Vienna, Vienna, Austria, 3 ReseaChem GmbH, Burgdorf, Switzerland, 4 Neuroscience Research, pRED, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland Background: 2,4,5-Trimethoxyamphetamine (TMA-2) is a potent psychedelic compound. Structurally related 4-alkyloxy-substituted 2,5-dimethoxyamphetamines and phenethylamine congeners (2C-O derivatives) have been described but their pharmacology Edited by: is mostly undefined. Therefore, we examined receptor binding and activation profiles of M. Foster Olive, these derivatives at monoamine receptors and transporters. Arizona State University, United States Methods: Receptor binding affinities were determined at the serotonergic 5-HT1A, 5-HT2A, Reviewed by: Luc Maroteaux, and 5-HT2C receptors, trace amine-associated receptor 1 (TAAR1), adrenergic α1 and INSERM U839 Institut du Fer à α2 receptors, dopaminergic D2 receptor, and at monoamine transporters, using target- Moulin, France Simon D. Brandt, transfected cells. Additionally, activation of 5-HT2A and 5-HT2B receptors and TAAR1 was Liverpool John Moores University, determined. Furthermore, we assessed monoamine transporter inhibition. United Kingdom Results: Both the phenethylamine and amphetamine derivatives (Ki = 8–1700 nM and *Correspondence: Matthias E. Liechti 61–4400 nM, respectively) bound with moderate to high affinities to the 5-HT2A receptor [email protected] with preference over the 5-HT1A and 5-HT2C receptors (5-HT2A/5-HT1A = 1.4–333 and Specialty section: 5-HT2A/5-HT2C = 2.1–14, respectively). -
Clifford G. Andrew, MD, Ph.D. Neurology Resident 1976-79
Clifford G. Andrew, M.D., Ph.D. Neurology Resident 1976-79; Neuromuscular Fellow 1979-80; Assistant Professor of Neurology 1980- 86; Currently: Assistant Professor of Neurology Part-time, Johns Hopkins University, Baltimore, Maryland, MD; [email protected]; website www.neurol.org My time at Hopkins came at an important crossroads in my life: having completed my MD/PhD (Biochemistry) at Duke’s Medical Scientist Training Program with mentor Stan Appel, honing my clinical skills for long, continuing career in Neurology. In 1976 the department had 4 professors: Daniel Drachman, John Freeman, Richard Johnson & Guy McKhann who amazed us with trans-Atlantic sailing. There were “young Turk” assistant professors Jack Griffin, and David Zee; and incoming resident Justin McArthur (1981). We learned to “See one, do one, and show one.” and “If you don’t get your work done in 24 hours you just have to stay up late!” During this time we moved laboratories, clinics, and wards to the Adolf Meyer Building and I learned three things: 1) art of compassionate care for patients; 2) the importance of applying rigorous science to evidence-based medicine (1998 Physicians’ Health Study II, 2008 Harvard Personal Genome Project PGP-84, and 2018 NIH All Of Us Research Precision Medicine; and 3) the importance of life beyond career: sailing the Chesapeake Bay in a 22-foot Bristol; raising 6 children, and 8 grandchildren; leadership in Cub, Boy, explorer Scouts, UU Church of Annapolis, teaching Hominid evolution at UUCA’s Camp Beagle “Vacation Darwin School”, USNA Secular Midshipmen, and UU Humanists & Naturalists; section thru-hiking the Appalachian Trail’s 2200 miles from GA to Me. -
Pharmacovigilance in Psychiatry Pharmacovigilance in Psychiatry
Edoardo Spina Gianluca Trifi rò Editors Pharmacovigilance in Psychiatry Pharmacovigilance in Psychiatry Edoardo Spina • Gianluca Trifi rò Editors Pharmacovigilance in Psychiatry Editors Edoardo Spina Gianluca Trifi rò Department of Clinical and Experimental Department of Clinical and Experimental Medicine Medicine University of Messina University of Messina Messina Messina Italy Italy ISBN 978-3-319-24739-7 ISBN 978-3-319-24741-0 (eBook) DOI 10.1007/978-3-319-24741-0 Library of Congress Control Number: 2015957257 Springer Cham Heidelberg New York Dordrecht London © Springer International Publishing Switzerland 2016 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfi lms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specifi c statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. -
Diverse Antidepressants Increase CDP-Diacylglycerol Production and Phosphatidylinositide Resynthesis in Depression-Relevant Regions of the Rat Brain
City University of New York (CUNY) CUNY Academic Works Publications and Research City College of New York 2008 Diverse Antidepressants Increase CDP-Diacylglycerol Production and Phosphatidylinositide Resynthesis in Depression-Relevant Regions of the Rat Brain Kimberly R. Tyeryar Laboratory of Integrative Neuropharmacology, University of Maryland School of Pharmacy Ashiwel S. Undieh CUNY City College Habiba OU Vongtau University of Maryland How does access to this work benefit ou?y Let us know! More information about this work at: https://academicworks.cuny.edu/cc_pubs/209 Discover additional works at: https://academicworks.cuny.edu This work is made publicly available by the City University of New York (CUNY). Contact: [email protected] See discussions, stats, and author profiles for this publication at: http://www.researchgate.net/publication/5633846 Diverse antidepressants increase CDP- diacylglycerol production and phosphatidylinositide resynthesis in depression- relevant regions of the rat brain ARTICLE in BMC NEUROSCIENCE · FEBRUARY 2008 Impact Factor: 2.67 · DOI: 10.1186/1471-2202-9-12 · Source: PubMed CITATIONS READS 11 26 3 AUTHORS: Kimberly Tyeryar Habiba Vongtau University of North Carolina at Chapel Hill University of Pittsburgh 10 PUBLICATIONS 305 CITATIONS 15 PUBLICATIONS 272 CITATIONS SEE PROFILE SEE PROFILE Ashiwel S Undieh Thomas Jefferson University 42 PUBLICATIONS 1,651 CITATIONS SEE PROFILE Available from: Ashiwel S Undieh Retrieved on: 04 December 2015 BMC Neuroscience BioMed Central Research article Open Access -
Major Depressive Disorder File
MAJOR DEPRESSIVE DISORDER MAJOR DEPRESSIVE DISORDER • Major depressive disorder (MDD) is a debilitating disease that is characterized by at least one discrete depressive episode lasting at least 2 weeks and involving clear-cut changes in mood, interests and pleasure, changes in cognition and vegetative symptoms • MDD is a heterogeneous disorder, and is often associated with other psychiatric conditions, including anxiety, eating disorders and drug addiction MAJOR DEPRESSIVE DISORDER • The symptoms of depression include emotional and biological components. Emotional symptoms include • Emotional symptoms include • Low mood, excessive rumination of negative thought, misery, apathy and pessimism • Low self-confidence: • feelings of guilt • inadequacy • ugliness • Indecisiveness, loss of motivation • Anhedonia, loss of reward • Biological symptoms include • Retardation of thought and action • Loss of libido • Sleep disturbance and loss of appetite MAJOR DEPRESSIVE DISORDER • Mechanisms/pathophysiology • Genetics • MDD is highly polygenic and involves many genes with small effects • Gene-environment interactions • The lack of consistent and replicated findings in genetic studies for MDD can at least partly be explained by the fact that relevant genetic variants confer an increased risk only in the presence of exposure to stressors and other adverse environmental circumstances • Environmental factors • There is a clear evidence of a dose– response relationship between the number and severity of adverse life events and the risk, severity and chronicity -
Corticosteroids Regulate Brain Hippocampal SHT,, Receptor Mrna Expression
The Journal of Neuroscience, March 1993, 13(3): 914-923 Corticosteroids Regulate Brain Hippocampal SHT,, Receptor mRNA Expression D. T. Chalmers, S. P. Kwak, A. Mansour, H. Akil, and S. J. Watson Mental Health Research Institute, University of Michigan, Ann Arbor, Michigan 48109 Using in situ hybridization techniques, the expression of ology of depressive illness and other affective disorders. In ad- 5-HT,, receptor mRNA was measured within the hippocam- dition to neuroendocrine function, serotonergic transmission is pal formation after bilateral adrenalectomy (ADX). After 24 implicated in normal and abnormal mental states (Eison, 1990) hr ADX, 5HT,, receptor mRNA expression was significantly and selective serotonergic compounds are clinically effective increased in all hippocampal subfields in ADX animals rel- antidepressants and anxiolytics (Cohn and Wilcox, 1985; Traber ative to sham-operated controls (SHAM). The magnitude of and Glaser, 1987). Thus, it is likely that the functional inter- the increase was most pronounced within CA2 (127%) and actions between the HPA system and the central serotonergic CA3/4 (94%)subfields of dorsal hippocampus, intermediate system may be significant, providing a biochemical basis for in the dentate gyrus (73%), and least within CA1 (60%). hormonally induced alterations in CNS circuits. Administration of exogenous cotticosterone (CORT) at the Corticosteroids have been shown to alter several elements of time of ADX maintained the level of 5-HT,, receptor mRNA serotonergic neurotransmission. Removal of circulating corti- expression within the range of SHAM animals. In vitro re- costeroids by adrenalectomy (ADX) results in anatomically spe- ceptor autoradiographic analysis of 5HT,, receptors in ad- cific decreases in indices of 5-HT metabolism, while stressful jacent sections from the same animals indicated a simul- procedures, which raise corticosteroid levels, produce corre- taneous increase in 5-HT,, binding throughout the sponding increases in 5-HT turnover (Curzon et al., 1972; Van hippocampus in response to ADX. -
Paving the Way for Therapy
Paving the Way for Therapy 2nd International Conference of the Trisomy 21 Research Society June 7-11, 2017 Feinberg Conference Center, Northwestern Memorial Hospital Chicago, IL USA Founding Sponsors of T21RS 1 Paving the Way for Therapy 2nd International Conference of the Trisomy 21 Research Society June 7-11, 2017 Feinberg Conference Center, Northwestern Memorial Hospital Chicago, IL USA Conference Organizers Roger Reeves, PhD Mara Dierssen, MD, PhD Johns Hopkins University School of CRG – Center for Genomic Medicine Regulation Jean Delabar, PhD John O’Bryan, PhD CNRS-ICM University of Illinois Chicago Scientific Program Committee Mara Dierssen, MD, PhD - Chair Anita Bhattacharyya, PhD CRG-Center for Genomic Regulation University of Wisconsin-Madison Cynthia Lemere, PhD Jean Delabar, PhD Harvard Medical School CNRS-ICM Dean Nizetic, MD, PhD Jorge Busciglio, PhD Nanyang Technological University University of California-Irvine Singapore Nicole Schupf, PhD, DrPH Pablo Caviedes, MD, PhD Columbia University Medical Center University of Chile Deny Menghini, PhD Bambino Gesu Children's Hospital 2 3 Annette Karmiloff-Smith Thesis Award Program COMPETITION FOR OUTSTANDING PH.D. THESIS Application Deadline: June 30, 2018 Prizes will be awarded for up to 2 outstanding doctoral dissertations. Each recipient will receive an honorarium of 1,000 Euros. The topic of the dissertation must be in the field of Down syndrome Eligibility Participation in the 2017 competition is limited to candidates who obtained the Ph.D. title during the period January 1, 2016-December 31, 2017. Applicants must be members of T21RS (www.t21rs.org/register). Required Documentation Documentation accompanying the application must be submitted exclusively in an email to [email protected] in PDF format and must be written in English.