Selegiline) in Monkeys*
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Neurotransmitter Resource Guide
NEUROTRANSMITTER RESOURCE GUIDE Science + Insight doctorsdata.com Doctor’s Data, Inc. Neurotransmitter RESOURCE GUIDE Table of Contents Sample Report Sample Report ........................................................................................................................................................................... 1 Analyte Considerations Phenylethylamine (B-phenylethylamine or PEA) ................................................................................................. 1 Tyrosine .......................................................................................................................................................................................... 3 Tyramine ........................................................................................................................................................................................4 Dopamine .....................................................................................................................................................................................6 3, 4-Dihydroxyphenylacetic Acid (DOPAC) ............................................................................................................... 7 3-Methoxytyramine (3-MT) ............................................................................................................................................... 9 Norepinephrine ........................................................................................................................................................................ -
Emerging Evidence for a Central Epinephrine-Innervated A1- Adrenergic System That Regulates Behavioral Activation and Is Impaired in Depression
Neuropsychopharmacology (2003) 28, 1387–1399 & 2003 Nature Publishing Group All rights reserved 0893-133X/03 $25.00 www.neuropsychopharmacology.org Perspective Emerging Evidence for a Central Epinephrine-Innervated a1- Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression ,1 1 1 1 1 Eric A Stone* , Yan Lin , Helen Rosengarten , H Kenneth Kramer and David Quartermain 1Departments of Psychiatry and Neurology, New York University School of Medicine, New York, NY, USA Currently, most basic and clinical research on depression is focused on either central serotonergic, noradrenergic, or dopaminergic neurotransmission as affected by various etiological and predisposing factors. Recent evidence suggests that there is another system that consists of a subset of brain a1B-adrenoceptors innervated primarily by brain epinephrine (EPI) that potentially modulates the above three monoamine systems in parallel and plays a critical role in depression. The present review covers the evidence for this system and includes findings that brain a -adrenoceptors are instrumental in behavioral activation, are located near the major monoamine cell groups 1 or target areas, receive EPI as their neurotransmitter, are impaired or inhibited in depressed patients or after stress in animal models, and a are restored by a number of antidepressants. This ‘EPI- 1 system’ may therefore represent a new target system for this disorder. Neuropsychopharmacology (2003) 28, 1387–1399, advance online publication, 18 June 2003; doi:10.1038/sj.npp.1300222 Keywords: a1-adrenoceptors; epinephrine; motor activity; depression; inactivity INTRODUCTION monoaminergic systems. This new system appears to be impaired during stress and depression and thus may Depressive illness is currently believed to result from represent a new target for this disorder. -
Medical Review Officer Manual
Department of Health and Human Services Substance Abuse and Mental Health Services Administration Center for Substance Abuse Prevention Medical Review Officer Manual for Federal Agency Workplace Drug Testing Programs EFFECTIVE OCTOBER 1, 2010 Note: This manual applies to Federal agency drug testing programs that come under Executive Order 12564 dated September 15, 1986, section 503 of Public Law 100-71, 5 U.S.C. section 7301 note dated July 11, 1987, and the Department of Health and Human Services Mandatory Guidelines for Federal Workplace Drug Testing Programs (73 FR 71858) dated November 25, 2008 (effective October 1, 2010). This manual does not apply to specimens submitted for testing under U.S. Department of Transportation (DOT) Procedures for Transportation Workplace Drug and Alcohol Testing Programs (49 CFR Part 40). The current version of this manual and other information including MRO Case Studies are available on the Drug Testing page under Medical Review Officer (MRO) Resources on the SAMHSA website: http://www.workplace.samhsa.gov Previous Versions of this Manual are Obsolete 3 Table of Contents Chapter 1. The Medical Review Officer (MRO)........................................................................... 6 Chapter 2. The Federal Drug Testing Custody and Control Form ................................................ 7 Chapter 3. Urine Drug Testing ...................................................................................................... 9 A. Federal Workplace Drug Testing Overview.................................................................. -
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. -
2-Phenylethylamine and Methamphetamine Enhance the Spinal Monosynaptic Reflex by Releasing Noradrenaline from the Terminals of Descending Fibers
Japan. J. Pharmacol. 55, 359-366 (1991) 359 2-Phenylethylamine and Methamphetamine Enhance the Spinal Monosynaptic Reflex by Releasing Noradrenaline from the Terminals of Descending Fibers Hideki Ono, Hiroyuki Ito and Hideomi Fukuda' Departmentof Toxicologyand Pharmacology,Faculty of Pharmaceutical Sciences, TheUniversity of Tokyo,Hongo 7-3-1, Bunkyo-ku, Tokyo 113, Japan 'Departmentof Pharmacology, Collegeof Pharmacy,Nihon University, 7-7-1Narashinodai, Funabashi, Chiba 274, Japan ReceivedJuly 28, 1990 AcceptedDecember 27, 1990 ABSTRACT Experiments were performed on spinalized rats transected at C1. In travenous administration of 2-phenylethylamine-HC1 (PEA-HC1) (0.3 and 1 mg/kg, i.v.) and methamphetamine-HC1 (MAP-HC1) (0.1 and 0.3 mg/kg, i.v.) increased the amplitude of the monosynaptic reflex (MSR). The increase of the MSR caused by PEA and MAP was antagonized by prazosin-HC1 and abolished by the pretreatment with reserpine (i.p.) and 6-hydroxydopamine (intracisternally, 14 days previously). A dopamine D, antagonist, SK&F 83566-HBr (0.01 mg/kg, i.v. ), and a D2 antagonist, YM-09151-2 (0.3 mg/kg, i.v.), did not antagonize the increasing effects produced by PEA and MAP. An inhibitor of type-B monoamine oxidase, (-)deprenyl-HC1 (1 mg/kg, i.v.), prolonged the effect of PEA but not that of MAP, suggesting that PEA alone, and not its metabolites, enhanced the MSR. These results suggest that PEA and MAP increase the amplitude of the MSR by releasing noradrenaline from the ter minals of descending noradrenergic fibers, and that PEA, an endogenous trace amine, has a mechanism of action similar to that of MAP. -
Dexmethylphenidate Hydrochloride Extended-Release Capsules These
DEXMETHYLPHENIDATE HYDROCHLORIDE- dexmethylphenidate hydrochloride capsule, extended release Granules Pharmaceuticals Inc. ---------- HIGHLIGHTS OF PRESCRIBING INFORMATION Dexmethylphenidate hydrochloride extended-release capsules These highlights do not include all the information needed to use DEXMETHYLPHENIDATE HYDROCHLORIDE EXTENDED-RELEASE CAPSULES safely and effectively. See full prescribing information for DEXMETHYLPHENIDATE HYDROCHLORIDE EXTENDED RELEASE CAPSULES. DEXMETHYLPHENIDATE HYDROCHLORIDE extended-release capsules, for oral use, CII Initial U.S. Approval: 2005 WARNING: ABUSE AND DEPENDENCE See full prescribing information for complete boxed warning. • CNS stimulants, including dexmethylphenidate hydrochloride extended-release, other methylphenidate-containing products, and amphetamines, have a high potential for abuse and dependence( 5.1, 9.2, 9.3). • Assess the risk of abuse prior to prescribing and monitor for signs of abuse and dependence while on therapy ( 5.1, 9.2). INDICATIONS AND USAGE Dexmethylphenidate hydrochloride extended-release capsules are a central nervous system (CNS) stimulant indicated for the treatment of Attention Deficit Hyperactivity Disorder (ADHD) ( 1) DOSAGE AND ADMINISTRATION • Patients new to methylphenidate: Recommended starting dose is 5 mg once daily for pediatric patients and 10 mg once daily for adults with or without food in the morning ( 2.2) • Patients currently on methylphenidate: Dexmethylphenidate hydrochloride extended-release dosage is half the current total daily dosage of methylphenidate -
Tyramine and Amyloid Beta 42: a Toxic Synergy
biomedicines Article Tyramine and Amyloid Beta 42: A Toxic Synergy Sudip Dhakal and Ian Macreadie * School of Science, RMIT University, Bundoora, VIC 3083, Australia; [email protected] * Correspondence: [email protected]; Tel.: +61-3-9925-6627 Received: 5 May 2020; Accepted: 27 May 2020; Published: 30 May 2020 Abstract: Implicated in various diseases including Parkinson’s disease, Huntington’s disease, migraines, schizophrenia and increased blood pressure, tyramine plays a crucial role as a neurotransmitter in the synaptic cleft by reducing serotonergic and dopaminergic signaling through a trace amine-associated receptor (TAAR1). There appear to be no studies investigating a connection of tyramine to Alzheimer’s disease. This study aimed to examine whether tyramine could be involved in AD pathology by using Saccharomyces cerevisiae expressing Aβ42. S. cerevisiae cells producing native Aβ42 were treated with different concentrations of tyramine, and the production of reactive oxygen species (ROS) was evaluated using flow cytometric cell analysis. There was dose-dependent ROS generation in wild-type yeast cells with tyramine. In yeast producing Aβ42, ROS levels generated were significantly higher than in controls, suggesting a synergistic toxicity of Aβ42 and tyramine. The addition of exogenous reduced glutathione (GSH) was found to rescue the cells with increased ROS, indicating depletion of intracellular GSH due to tyramine and Aβ42. Additionally, tyramine inhibited the respiratory growth of yeast cells producing GFP-Aβ42, while there was no growth inhibition when cells were producing GFP. Tyramine was also demonstrated to cause increased mitochondrial DNA damage, resulting in the formation of petite mutants that lack respiratory function. -
Recommended Methods for the Identification and Analysis Of
Vienna International Centre, P.O. Box 500, 1400 Vienna, Austria Tel: (+43-1) 26060-0, Fax: (+43-1) 26060-5866, www.unodc.org RECOMMENDED METHODS FOR THE IDENTIFICATION AND ANALYSIS OF AMPHETAMINE, METHAMPHETAMINE AND THEIR RING-SUBSTITUTED ANALOGUES IN SEIZED MATERIALS (revised and updated) MANUAL FOR USE BY NATIONAL DRUG TESTING LABORATORIES Laboratory and Scientific Section United Nations Office on Drugs and Crime Vienna RECOMMENDED METHODS FOR THE IDENTIFICATION AND ANALYSIS OF AMPHETAMINE, METHAMPHETAMINE AND THEIR RING-SUBSTITUTED ANALOGUES IN SEIZED MATERIALS (revised and updated) MANUAL FOR USE BY NATIONAL DRUG TESTING LABORATORIES UNITED NATIONS New York, 2006 Note Mention of company names and commercial products does not imply the endorse- ment of the United Nations. This publication has not been formally edited. ST/NAR/34 UNITED NATIONS PUBLICATION Sales No. E.06.XI.1 ISBN 92-1-148208-9 Acknowledgements UNODC’s Laboratory and Scientific Section wishes to express its thanks to the experts who participated in the Consultative Meeting on “The Review of Methods for the Identification and Analysis of Amphetamine-type Stimulants (ATS) and Their Ring-substituted Analogues in Seized Material” for their contribution to the contents of this manual. Ms. Rosa Alis Rodríguez, Laboratorio de Drogas y Sanidad de Baleares, Palma de Mallorca, Spain Dr. Hans Bergkvist, SKL—National Laboratory of Forensic Science, Linköping, Sweden Ms. Warank Boonchuay, Division of Narcotics Analysis, Department of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand Dr. Rainer Dahlenburg, Bundeskriminalamt/KT34, Wiesbaden, Germany Mr. Adrian V. Kemmenoe, The Forensic Science Service, Birmingham Laboratory, Birmingham, United Kingdom Dr. Tohru Kishi, National Research Institute of Police Science, Chiba, Japan Dr. -
Serotonin Syndrome How to Avoid, Identify, &
Serotonin syndrome How to avoid, identify, & As the list of serotonergic agents grows, recognizing hyperthermic states and potentially dangerous drug combinations is critical to our patients’ safety. 14 Current VOL. 2, NO. 5 / MAY 2003 p SYCHIATRY Current p SYCHIATRY treat dangerous drug interactions Harvey Sternbach, MD Clinical professor of psychiatry UCLA Neuropsychiatric Institute Los Angeles, CA romptly identifying serotonin syn- drome and acting decisively can keep side effects at the mild end of the spec- Ptrum. Symptoms of this potentially dangerous syndrome range from minimal in patients starting selective serotonin reuptake inhibitors (SSRIs) to fatal in those combining monoamine oxidase inhibitors (MAOIs) with serotonergic agents. This article presents the latest evidence on how to: • reduce the risk of serotonin syndrome • recognize its symptoms • and treat patients with mild to life- threatening symptoms. WHAT IS SEROTONIN SYNDROME? Serotonin syndrome is characterized by changes in autonomic, neuromotor, and cognitive-behav- ioral function (Table 1) triggered by increased serotonergic stimulation. It typically results from pharmacodynamic and/or pharmacokinetic in- teractions between drugs that increase serotonin activity.1,2 continued VOL. 2, NO. 5 / MAY 2003 15 Serotonin Table 1 activity or reduced ability to How to recognize serotonin syndrome secrete endothelium-derived nitric oxide may diminish the System Clinical signs and symptoms ability to metabolize serotonin.2 Autonomic Diaphoresis, hyperthermia, hypertension, tachycardia, pupillary dilatation, nausea, POTENTIALLY DANGEROUS diarrhea, shivering COMBINATIONS Neuromotor Hyperreflexia, myoclonus, restlessness, MAOIs. Serotonin syndrome tremor, incoordination, rigidity, clonus, has been reported as a result of teeth chattering, trismus, seizures interactions between MAOIs— Cognitive-behavioral Confusion, agitation, anxiety, hypomania, including selegiline and insomnia, hallucinations, headache reversible MAO-A inhibitors (RIMAs)—and various sero- tonergic compounds. -
Evidence That Formulations of the Selective MAO-B Inhibitor, Selegiline, Which Bypass First-Pass Metabolism, Also Inhibit MAO-A in the Human Brain
BNL-107759-2015-JA Evidence that formulations of the selective MAO-B inhibitor, selegiline, which bypass first-pass metabolism, also inhibit MAO-A in the human brain Joanna S. Fowler1, Jean Logan2, Nora D. Volkow3,4, Elena Shumay4, Fred McCall-Perez5, Michelle Gilmor7, Millard Jayne4, Gene-Jack Wang4, David L. Alexoff1, Karen Apelskog-Torres4, Barbara Hubbard1, Pauline Carter1, Payton King1, Stanley Fahn6, Frank Telang4, Colleen Shea1, Youwen Xu1, Lisa Muench4 1Biosciences Department, Brookhaven National Laboratory, Upton, NY 11973, USA 2New York University Langone Medical Center, New York, NY 10016, USA 3National Institute on Drug Abuse, Bethesda, MD, USA 4National Institute on Alcohol Abuse and Alcoholism, Bethesda MD, USA 5Targeted Medical Pharma Inc, Los Angeles, CA 90077, USA 6Novartis Pharmaceuticals, East Hanover, NJ 07936, USA 7Neurological Institute, Columbia University, New York, NY, USA Submitted to Neuropsychopharmacology July 2014 Biological, Environmental and Climate Sciences Department Brookhaven National Laboratory U.S. Department of Energy Office of Science Office of Biological and Environmental Research Notice: This manuscript has been authored by employees of Brookhaven Science Associates, LLC under Contract No. DE-AC02-98CH10886 with the U.S. Department of Energy. The publisher by accepting the manuscript for publication acknowledges that the United States Government retains a non-exclusive, paid-up, irrevocable, world-wide license to publish or reproduce the published form of this manuscript, or allow others to do -
212102Orig1s000
CENTER FOR DRUG EVALUATION AND RESEARCH APPLICATION NUMBER: 212102Orig1s000 OTHER REVIEW(S) Department of Health and Human Services Food and Drug Administration Center for Drug Evaluation and Research | Office of Surveillance and Epidemiology (OSE) Epidemiology: ARIA Sufficiency Date: June 29, 2020 Reviewer: Silvia Perez-Vilar, PharmD, PhD Division of Epidemiology I Team Leader: Kira Leishear, PhD, MS Division of Epidemiology I Division Director: CAPT Sukhminder K. Sandhu, PhD, MPH, MS Division of Epidemiology I Subject: ARIA Sufficiency Memo for Fenfluramine-associated Valvular Heart Disease and Pulmonary Arterial Hypertension Drug Name(s): FINTEPLA (Fenfluramine hydrochloride, ZX008) Application Type/Number: NDA 212102 Submission Number: 212102/01 Applicant/sponsor: Zogenix, Inc. OSE RCM #: 2020-953 The original ARIA memo was dated June 23, 2020. This version, dated June 29, 2020, was amended to include “Assess a known serious risk” as FDAAA purpose (per Section 505(o)(3)(B)) to make it consistent with the approved labeling. The PMR development template refers to the original memo, dated June 23, 2020. Page 1 of 13 Reference ID: 46331494640015 EXECUTIVE SUMMARY (place “X” in appropriate boxes) Memo type -Initial -Interim -Final X X Source of safety concern -Peri-approval X X -Post-approval Is ARIA sufficient to help characterize the safety concern? Safety outcome Valvular Pulmonary heart arterial disease hypertension (VHD) (PAH) -Yes -No X X If “No”, please identify the area(s) of concern. -Surveillance or Study Population X X -Exposure -Outcome(s) of Interest X X -Covariate(s) of Interest X X -Surveillance Design/Analytic Tools Page 2 of 13 Reference ID: 46331494640015 1. -
Anticonvulsants Antipsychotics Benzodiazepines/Anxiolytics ADHD
Anticonvulsants Antidepressants Generic Name Brand Name Generic Name Brand Name Carbamazepine Tegretol SSRI Divalproex Depakote Citalopram Celexa Lamotrigine Lamictal Escitalopram Lexapro Topirimate Topamax Fluoxetine Prozac Fluvoxamine Luvox Paroxetine Paxil Antipsychotics Sertraline Zoloft Generic Name Brand Name SNRI Typical Desvenlafaxine Pristiq Chlorpromazine Thorazine Duloextine Cymbalta Fluphenazine Prolixin Milnacipran Savella Haloperidol Haldol Venlafaxine Effexor Perphenazine Trilafon SARI Atypical Nefazodone Serzone Aripiprazole Abilify Trazodone Desyrel Clozapine Clozaril TCA Lurasidone Latuda Clomimpramine Enafranil Olanzapine Zyprexa Despiramine Norpramin Quetiapine Seroquel Nortriptyline Pamelor Risperidone Risperal MAOI Ziprasidone Geodon Phenylzine Nardil Selegiline Emsam Tranylcypromine Parnate Benzodiazepines/Anxiolytics DNRI Generic Name Brand Name Bupropion Wellbutrin Alprazolam Xanax Clonazepam Klonopin Sedative‐Hypnotics Lorazepam Ativan Generic Name Brand Name Diazepam Valium Clonidine Kapvay Buspirone Buspar Eszopiclone Lunesta Pentobarbital Nembutal Phenobarbital Luminal ADHD Medicines Zaleplon Sonata Generic Name Brand Name Zolpidem Ambien Stimulant Amphetamine Adderall Others Dexmethylphenidate Focalin Generic Name Brand Name Dextroamphetamine Dexedrine Antihistamine Methylphenidate Ritalin Non‐stimulant Diphenhydramine Bendryl Atomoxetine Strattera Anti‐tremor Guanfacine Intuniv Benztropine Cogentin Mood stabilizer (bipolar treatment) Lithium Lithane Never Mix, Never Worry: What Clinicians Need to Know about