Synthesis, 142 Termination of Action, 142–143 See Also Serotonin

Total Page:16

File Type:pdf, Size:1020Kb

Synthesis, 142 Termination of Action, 142–143 See Also Serotonin Cambridge University Press 978-1-107-02598-1 — Stahl's Essential Psychopharmacology 4th Edition Index More Information Index 5HT (5-hydroxytryptamine) acetaminophen, 340 alpha 1 adrenergic antagonists synthesis, 142 acetylation of histones, 24 atypical antipsychotics, 173 termination of action, 142–143 acetylcholine, 5 alpha 2 antagonists, 317–322 See also serotonin. as brain’s own nicotine, 543 alpha 2 delta ligands 5HT1A receptor partial agonists basis for cholinesterase treatment as anxiolytics, 403–405 atypical antipsychotics, 156–159 of dementia, 522–528 alpha 2A adrenergic agonists vilazodone, 300–302 cholinergic pathways, 524 ADHD treatment, 495–499 5HT1B/D receptors cholinergic receptors, 523–528 alpha-melanocyte stimulating effects of atypical antipsychotics, precursors, 524 hormone (alpha-MSH), 565 159–160 acetylcholine transporters, 523 alprazolam, 5, 49 terminal autoreceptors, 159–160 acetylcholine vesicular transporter, 29 Alzheimer’s dementia, 504 5HT2A receptor antagonists, 318 acetylcholinesterase, 46, 522–525 and psychosis, 79 atypical antipsychotic actions, Adapin, 342 Alzheimer’s disease 142–156 adenosine antagonist acetylcholine as target for current effects on dopamine D2 receptors, caffeine, 469 symptomatic treatment, 522–527 151–156 adiponectin, 565 aggressive and hostile symptoms, 85 effects on extrapyramidal adolescents amyloid as target of disease- symptoms, 150 bipolar disorder, 386 modifying treatment, 520–523 effects on prolactin levels, mania, 386 amyloid cascade hypothesis, 150–151 mood stabilizer selection, 386 505–509 stimulating downstream dopamine affective disorders. See mood disorders. basis for cholinesterase treatments, release, 142–150 aggression 522–528 5HT2A receptors disorders associated with, 85 beta amyloid plaques, 505–509 blocking downstream dopamine impulsive–compulsive behavior in beta secretase inhibitors, 522 release, 142–150 psychiatric disorders, 574 biomarker-enhanced early 5HT2C receptor antagonists, 313–318 in schizophrenia, 84 detection, 521 fluoxetine, 297 agomelatine, 159, 313–317, 457 biomarkers, 516–518 5HT2C receptors agonist action causes, 503–505 effects of atypical antipsychotics, G-protein-linked receptors, 35–36 cholinergic deficiency hypothesis 159–162 ligand-gated ion channels, 56 of amnesia in, 525 role in obesity treatment, 159 agonist spectrum cholinesterase inhibitors, 525–527 5HT3 receptor antagonists, 318–322, G-protein-linked receptors, 35–43 clinical features, 503–505 500, 559 ligand-gated ion channels, 56–64 cognitive symptoms, 85 5HT3 receptors agoraphobia diagnosis, 503–505 effects of atypical antipsychotics, in children, 386 diagnostic categories for 162 agouti-related peptide, 565 Alzheimer’s dementia, 519–520 5HT6 receptor antagonists, 500 agouti-related protein, 565 donepezil, 529 5HT6 receptors akathisia, 95, 168 galantamine, 527 effects of atypical antipsychotics, Akiskal, Hagop, 243 gamma secretase inhibitors, 162 AKT (kinase enzyme) 521–522 5HT7 receptors in schizophrenia, 128 genetic studies, 509 effects of atypical antipsychotics, alcohol dependence, 551–559 glutamate hypothesis of cognitive 162–165 alcoholism treatment, 468 deficiency, 527–534 allodynia, 425 immunotherapy research, 521 Abeta peptides allosteric modulation memantine, 527–531 role in Alzheimer’s disease, 505, ligand-gated ion channels, 65–67 neurofibrillary tangles, 505–509 507, 509 almorexant (SB649868), 463 neuroimaging biomarkers, 517–518 ABT560, 500 alogia pathology, 503–505 acamprosate, 385, 417, 556–558 in schizophrenia, 82 positive symptoms, 85 591 © in this web service Cambridge University Press www.cambridge.org Cambridge University Press 978-1-107-02598-1 — Stahl's Essential Psychopharmacology 4th Edition Index More Information Index Alzheimer’s disease (cont.) amyloid precursor protein (APP) antidepressant classes possible Alzheimer’s dementia role in Alzheimer’s disease, 5HT2C antagonism, 313–317 category, 519–520 505–507, 509 alpha 2 antagonists, 317–322 possible benefits of lithium, 372 amyotrophic lateral sclerosis circadian rhythm resynchronizer, probable Alzheimer’s dementia (ALS), 379 313–317 category, 519–520 Anafranil, 342 melatonergic action, 313–317 prodromal stage, 515–519 analgesics monoamine oxidase inhibitors range of proposed targets, 533–536 interactions with MAOIs, 340 (MAOIs), 326–342 risk factors for disease anandamide, 5, 543, 561 monoamine transporter blockers, progression, 515 anatomical basis of 289–346 risk related to Apo-E, 509–510 neurotransmission, 1–2 norepinephrine–dopamine rivastigmine, 526–527 anatomically addressed nervous reuptake inhibitors (NDRIs), role of Abeta peptides, 505, 507, 509 system, 1–2 309–312 role of amyloid precursor protein anesthetics selective norepinephrine reuptake (APP), 505–507, 509 interactions with MAOIs, 335 inhibitors (NRIs), 312–313 role of pathological tau, 508 “angel dust”. See phencyclidine (PCP) serotonin antagonist/reuptake search for a vaccine, 521 anhedonia inhibitors (SARIs), 322–326 targeting glutamate, 527–531 in schizophrenia, 82 serotonin–norepinephrine testing of potential treatments, anorexia nervosa, 564 reuptake inhibitors (SNRIs), 533–536 antagonist action 302–309 treatments for psychiatric and G-protein-linked receptors, 36–37 serotonin partial agonist- behavioral symptoms, 531–533 ligand-gated ion channels, 57–59 reuptake inhibitors (SPARIs), Alzheimer’s disease stages, 510–511 anticholinergics, 523 300–302 amyloidosis with anticonvulsants, 73 serotonin selective reuptake neurodegeneration and cognitive as mood stabilizers, 373–380 inhibitors (SSRIs), 290–300 decline, 519–520 antidepressant action, 47 tricyclic antidepressants, 312, amyloidosis with some atypical antipsychotics, 169–172 342–346 neurodegeneration, 515–519 comparison with placebo in clinical antidepressant-induced bipolar asymptomatic amyloidosis, 511–515 trials, 285 disorder, 382 dementia stage, 519–520 debate over efficacy, 285–287 antidepressant-induced mood distinction of MCI from normal definition of a treatment response, disorders, 247–250 aging, 515–519 285 antidepressant “poop-out”, 245 first stage (preclinical), 511–515 discovery of, 6 antidepressant selection mild cognitive impairment (MCI), disease progression in major arousal combos, 365 515–519 depression, 289 based on genetic testing, 361–362 presymptomatic stage, 511–515 effects throughout the life based on weight of the evidence, second stage, 515–519 cycle, 289 361–362 symptomatic predementia stage, efficacy in clinical trials, 285–287 breastfeeding patient, 361 515–519 failure to achieve remission, 287 California rocket fuel (SNRI plus third (final) stage, 519–520 general principles, 285–289 mirtazapine), 363 amenorrhea, 95 goal of sustained remission, 285 combination therapies for amisulpride, 168 importance of achieving remission, major depressive disorder, pharmacologic properties, 212 289 362–365 amitifidine (triple reuptake inhibitor), in “real world” trials, 289 combination therapies for 365 STAR-D trial of antidepressants, treatment-resistant depression, amitriptyline, 6, 342 287 362–365 amoxapine, 162, 342 antidepressant augmenting agents, depression treatment strategy, AMPA PAMs, 228 346–353 284–285 AMPA receptor modulators, 228 brain stimulation techniques, equipoise situation, 361–362 AMPA receptors, 101–102 350–352 evidence-based selection, AMPAkines, 228, 500 buspirone, 301–302 353–354 amphetamine, 34, 327, 547 deep brain stimulation (DBS), for pregnant patients, 357–361 ADHD treatment, 490–491 351–352 for women based on life-cycle brain’s own (dopamine), 543 electroconvulsive therapy (ECT), 350 stage, 357 wake-promoting agent, 468 L-methylfolate, 346–350 for women of childbearing age, amygdala, 122 psychotherapy as an epigenetic 357–361 fear response, 392–395 “drug”, 352–353 postpartum patient, 361 neurobiology of fear, 392–395 SAMe (S-adenosyl-methionine), 350 symptom-based approach, neuroimaging in schizophrenia, thyroid hormones, 350 354–357 122–126 transcranial magnetic stimulation triple action combination role in fear conditioning, 409–411 (TMS), 350–351 (SSRI/SNRI/NDRI), 362–363 592 © in this web service Cambridge University Press www.cambridge.org Cambridge University Press 978-1-107-02598-1 — Stahl's Essential Psychopharmacology 4th Edition Index More Information Index antidepressants in development anxious self-punishment and blame late-onset type, 484 CRF1 (corticotrophin-releasing in depressive psychosis, 80 selective inattention symptom, factor) antagonists, 365 apathy 474 future treatments for mood in depressive psychosis, 80 symptoms, 471–475 disorders, 365–366 ApoE (apolipoprotein E) attention deficit hyperactivity disorder glucocorticoid antagonists, 365 and Alzheimer’s disease risk, (ADHD) treatment multimodal agents, 365–367 509–510 alpha 2A adrenergic agonists, NMDA blockade, 365–366 appetite regulation 495–499 serotonin–norepinephrine– neurobiological basis, 564 amphetamine, 490–491 dopamine reuptake inhibitors aripiprazole, 49–50, 159, 162, atomoxetine, 493–495 (SNDRIs), 365 168–169, 171, 300, 383 DAT target for stimulant drugs, triple reuptake inhibitors (TRIs), 365 metabolic risk, 173 491–496 vasopressin 1B antagonists, 365 pharmacologic properties, 202–210 differences in children, adolescents antihistamines, 335 armodafinil and adults, 484–487 antimanic actions in combinations of mood stabilizers, future treatments, 500–502 atypical antipsychotics, 171 385 general principles of stimulant antipsychotics, 47, 129–130 mode of action, 468 treatment, 487–490 as mood stabilizers, 373–381 mood-stabilizing properties,
Recommended publications
  • 4695389.Pdf (3.200Mb)
    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.
    [Show full text]
  • Homology Models of Melatonin Receptors: Challenges and Recent Advances
    Int. J. Mol. Sci. 2013, 14, 8093-8121; doi:10.3390/ijms14048093 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Review Homology Models of Melatonin Receptors: Challenges and Recent Advances Daniele Pala 1, Alessio Lodola 1, Annalida Bedini 2, Gilberto Spadoni 2 and Silvia Rivara 1,* 1 Dipartimento di Farmacia, Università degli Studi di Parma, Parco Area delle Scienze 27/A, 43124 Parma, Italy; E-Mails: [email protected] (D.P.); [email protected] (A.L.) 2 Dipartimento di Scienze Biomolecolari, Università degli Studi di Urbino “Carlo Bo”, Piazza Rinascimento 6, I-61029 Urbino, Italy; E-Mails: [email protected] (A.B.); [email protected] (G.S.) * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +39-0521-905-061; Fax: +39-0521-905-006. Received: 7 March 2013; in revised form: 28 March 2013 / Accepted: 28 March 2013 / Published: 12 April 2013 Abstract: Melatonin exerts many of its actions through the activation of two G protein-coupled receptors (GPCRs), named MT1 and MT2. So far, a number of different MT1 and MT2 receptor homology models, built either from the prototypic structure of rhodopsin or from recently solved X-ray structures of druggable GPCRs, have been proposed. These receptor models differ in the binding modes hypothesized for melatonin and melatonergic ligands, with distinct patterns of ligand-receptor interactions and putative bioactive conformations of ligands. The receptor models will be described, and they will be discussed in light of the available information from mutagenesis experiments and ligand-based pharmacophore models.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • File Download
    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.
    [Show full text]
  • ANTIDEPRESSANTS in USE in CLINICAL PRACTICE Mark Agius1 & Hannah Bonnici2 1Clare College, University of Cambridge, Cambridge, UK 2Hospital Pharmacy St
    Psychiatria Danubina, 2017; Vol. 29, Suppl. 3, pp 667-671 Conference paper © Medicinska naklada - Zagreb, Croatia ANTIDEPRESSANTS IN USE IN CLINICAL PRACTICE Mark Agius1 & Hannah Bonnici2 1Clare College, University of Cambridge, Cambridge, UK 2Hospital Pharmacy St. James Hospital Malta, Malta SUMMARY The object of this paper, rather than producing new information, is to produce a useful vademecum for doctors prescribing antidepressants, with the information useful for their being prescribed. Antidepressants need to be seen as part of a package of treatment for the patient with depression which also includes psychological treatments and social interventions. Here the main Antidepressant groups, including the Selective Serotonin uptake inhibiters, the tricyclics and other classes are described, together with their mode of action, side effects, dosages. Usually antidepressants should be prescribed for six months to treat a patient with depression. The efficacy of anti-depressants is similar between classes, despite their different mechanisms of action. The choice is therefore based on the side-effects to be avoided. There is no one ideal drug capable of exerting its therapeutic effects without any adverse effects. Increasing knowledge of what exactly causes depression will enable researchers not only to create more effective antidepressants rationally but also to understand the limitations of existing drugs. Key words: antidepressants – depression - psychological therapies - social therapies * * * * * Introduction Monoamine oxidase (MAO) inhibitors í Non-selective Monoamine Oxidase Inhibitors Depression may be defined as a mood disorder that í Selective Monoamine Oxidase Type A inhibitors negatively and persistently affects the way a person feels, thinks and acts. Common signs include low mood, Atypical Anti-Depressants and other classes changes in appetite and sleep patterns and loss of inte- rest in activities that were once enjoyable.
    [Show full text]
  • Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-Glcnacylation, Acetyl-Coa and Melatonergic Pathway in Regulat
    International Journal of Molecular Sciences Review Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-GlcNAcylation, Acetyl-CoA and Melatonergic Pathway in Regulating Dynamic Metabolic Interactions across Cell Types—Tumour Microenvironment and Metabolism George Anderson Clinical Research Communications (CRC) Scotland & London, Eccleston Square, London SW1V 6UT, UK; [email protected] Abstract: This article reviews the dynamic interactions of the tumour microenvironment, highlight- ing the roles of acetyl-CoA and melatonergic pathway regulation in determining the interactions between oxidative phosphorylation (OXPHOS) and glycolysis across the array of cells forming the tumour microenvironment. Many of the factors associated with tumour progression and immune resistance, such as yin yang (YY)1 and glycogen synthase kinase (GSK)3β, regulate acetyl-CoA and the melatonergic pathway, thereby having significant impacts on the dynamic interactions of the different types of cells present in the tumour microenvironment. The association of the aryl hydrocarbon receptor (AhR) with immune suppression in the tumour microenvironment may be mediated by the AhR-induced cytochrome P450 (CYP)1b1-driven ‘backward’ conversion of mela- tonin to its immediate precursor N-acetylserotonin (NAS). NAS within tumours and released from tumour microenvironment cells activates the brain-derived neurotrophic factor (BDNF) receptor, TrkB, thereby increasing the survival and proliferation of cancer stem-like cells. Acetyl-CoA is a cru- Citation:
    [Show full text]
  • 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).
    [Show full text]
  • Novel Melatonin MT1 Receptor Agonists As Antidepressants
    Novel melatonin MT1 receptor agonists as antidepressants: In vivo electrophysiological and behavioural characterization Ada R. Posner Degree of Master of Science Neurobiological Psychiatry Unit Department of Psychiatry Faculty of Medicine McGill University Montreal, Quebec, Canada April, 2015 A thesis submitted to McGill University in partial fulfillment of the requirements of the degree of Master of Science in Psychiatry Copyright Ada R. Posner, 2015 Table of Contents Table of Contents ................................................................................................ 2 Abstract ............................................................................................................... 3 Résumé ............................................................................................................... 5 Acknowledgements ............................................................................................. 7 Preface & Contribution of Authors ...................................................................... 8 Abbreviations ...................................................................................................... 9 Introduction ....................................................................................................... 14 Melatonin ...................................................................................................... 14 Sites and mechanisms of melatonin action: receptors ................................. 17 Localization and distribution of melatonin receptors in the brain
    [Show full text]
  • Α2 Adrenergic Receptor Trafficking As a Therapeutic Target in Antidepressant Drug Action
    CHAPTER NINE α2 Adrenergic Receptor Trafficking as a Therapeutic Target in Antidepressant Drug Action Christopher Cottingham*,1, Craig J. Ferryman*, Qin Wang†,1 *Department of Biology and Chemistry, Morehead State University, Morehead, Kentucky, USA †Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA 1Corresponding authors: e-mail address: [email protected]; [email protected] Contents 1. Introduction 207 2. Physiological Basis for Studying α2AAR Trafficking in Depression 209 3. Arrestin-Biased Regulation of the α2AAR by the TCA Drug Class 211 4. Therapeutic Implications 216 References 219 Abstract Antidepressant drugs remain poorly understood, especially with respect to pharmaco- logical mechanisms of action. This lack of knowledge results from the extreme complex- ity inherent to psychopharmacology, as well as to a corresponding lack of knowledge regarding depressive disorder pathophysiology. While the final analysis is likely to be multifactorial and heterogeneous, compelling evidence exists for upregulation of brain α2 adrenergic receptors (ARs) in depressed patients. This evidence has sparked a line of research into actions of a particular antidepressant drug class, the tricyclic antidepres- sants (TCAs), as direct ligands at α2AARs. Our findings, as outlined herein, demonstrate that TCAs function as arrestin-biased ligands at α2AARs. Importantly, TCA-induced α2AAR/arrestin recruitment leads to receptor endocytosis and downregulation of α2AAR expression with prolonged exposure. These findings represent a novel mecha- nism linking α2AR trafficking with antidepressant pharmacology. 1. INTRODUCTION Psychopharmacology is an exceedingly intricate discipline, aiming as it does to modulate human emotion, behavior, and other complex cognitive processes. Although our understanding of brain–behavior relationships has # Progress in Molecular Biology and Translational Science, Volume 132 2015 Elsevier Inc.
    [Show full text]
  • 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.
    [Show full text]
  • 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
    [Show full text]