Gabab Regulation of Methamphetamine-Induced Associative Learning
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Journal of Biological Rhythms Official Publication of the Society for Research on Biological Rhythms
Journal of Biological Rhythms Official Publication of the Society for Research on Biological Rhythms Volume 16, Issue 6 December 2001 EDITORIAL Pebbles of Truth 515 Martin Zatz FEATURE Review Clockless Yeast and the Gears of the Clock: How Do They Mesh? 516 Ruben Baler ARTICLES Resetting of the Circadian Clock by Phytochromes 523 and Cryptochromes in Arabidopsis Marcelo J. Yanovsky, M. Agustina Mazzella, Garry C. Whitelam, and Jorge J. Casal Distinct Pharmacological Mechanisms Leading to c-fos 531 Gene Expression in the Fetal Suprachiasmatic Nucleus Lauren P. Shearman and David R. Weaver Daily Novel Wheel Running Reorganizes and 541 Splits Hamster Circadian Activity Rhythms Michael R. Gorman and Theresa M. Lee Temporal Reorganization of the Suprachiasmatic Nuclei 552 in Hamsters with Split Circadian Rhythms Michael R. Gorman, Steven M. Yellon, and Theresa M. Lee Light-Induced Resetting of the Circadian Pacemaker: 564 Quantitative Analysis of Transient versus Steady-State Phase Shifts Kazuto Watanabe, Tom Deboer, and Johanna H. Meijer Temperature Cycles Induce a Bimodal Activity Pattern in Ruin Lizards: 574 Masking or Clock-Controlled Event? A Seasonal Problem Augusto Foà and Cristiano Bertolucci LETTER Persistence of Masking Responses to Light in Mice Lacking Rods and Cones 585 N. Mrosovsky, Robert J. Lucas, and Russell G. Foster MEETING Eighth Meeting of the Society for Research on Biological Rythms 588 Index 589 Journal of Biological Rhythms Official Publication of the Society for Research on Biological Rhythms EDITOR-IN-CHIEF Martin Zatz FEATURES EDITORS ASSOCIATE EDITORS Larry Morin Michael Hastings SUNY, Stony Brook University of Cambridge Anna Wirz-Justice Ken-Ichi Honma University of Basel Hokkaido Univ School Medicine Michael Young Rockefeller University EDITORIAL BOARD Josephine Arendt Terry Page University of Surrey Vanderbilt University Charles A. -
A Review of Effective ADHD Treatment Devin Hilla Grand Valley State University, [email protected]
Grand Valley State University ScholarWorks@GVSU Honors Projects Undergraduate Research and Creative Practice 12-2015 Changing Behavior, Brain Differences, or Both? A Review of Effective ADHD Treatment Devin Hilla Grand Valley State University, [email protected] Follow this and additional works at: http://scholarworks.gvsu.edu/honorsprojects Part of the Medicine and Health Sciences Commons Recommended Citation Hilla, Devin, "Changing Behavior, Brain Differences, or Both? A Review of Effective ADHD Treatment" (2015). Honors Projects. 570. http://scholarworks.gvsu.edu/honorsprojects/570 This Open Access is brought to you for free and open access by the Undergraduate Research and Creative Practice at ScholarWorks@GVSU. It has been accepted for inclusion in Honors Projects by an authorized administrator of ScholarWorks@GVSU. For more information, please contact [email protected]. Running Head: EFFECTIVE ADHD TREATMENT 1 Changing Behavior, Brain Differences, or Both? A Review of Effective ADHD Treatment Devin Hilla Grand Valley State University Honors Senior Thesis EFFECTIVE ADHD TREATMENT 2 Abstract Much debate exists over the proper course of treatment for individuals with attention- deficit/hyperactivity disorder (ADHD). Stimulant medications, such as methylphenidate (e.g., Ritalin) and amphetamine (e.g., Adderall), have been shown to be effective in managing ADHD symptoms. More recently, non-stimulant medications, such as atomoxetine (e.g., Strattera), clonidine (e.g., Kapvay), and guanfacine (e.g., Intuniv), have provided a pharmacological alternative with potentially lesser side effects than stimulants. Behavioral therapies, like behavioral parent training, behavioral classroom management, and behavioral peer interventions, have shown long-term benefits for children with ADHD; however, the success of the short-term management of ADHD symptoms is not as substantial when compared with stimulant medications. -
Specifications of Approved Drug Compound Library
Annexure-I : Specifications of Approved drug compound library The compounds should be structurally diverse, medicinally active, and cell permeable Compounds should have rich documentation with structure, Target, Activity and IC50 should be known Compounds which are supplied should have been validated by NMR and HPLC to ensure high purity Each compound should be supplied as 10mM solution in DMSO and at least 100µl of each compound should be supplied. Compounds should be supplied in screw capped vial arranged as 96 well plate format. -
Download Product Insert (PDF)
Product Information Fendiline (hydrochloride) Item No. 17295 CAS Registry No.: 13636-18-5 Formal Name: γ-phenyl-N-(1-phenylethyl)- benzenepropanamine, monohydrochloride MF: C23H25N • HCl FW: 351.9 N Purity: ≥95% H Stability: ≥2 years at -20°C Supplied as: A crystalline solid • HCl Laboratory Procedures For long term storage, we suggest that fendiline (hydrochloride) be stored as supplied at -20°C. It should be stable for at least two years. Fendiline (hydrochloride) is supplied as a crystalline solid. A stock solution may be made by dissolving the fendiline (hydrochloride) in the solvent of choice. Fendiline (hydrochloride) is soluble in organic solvents such as ethanol, DMSO, and dimethyl formamide, which should be purged with an inert gas. The solubility of fendiline (hydrochloride) in these solvents is approximately 15, 30, and 20 mg/ml, respectively. Further dilutions of the stock solution into aqueous buffers or isotonic saline should be made prior to performing biological experiments. Ensure that the residual amount of organic solvent is insignificant, since organic solvents may have physiological effects at low concentrations. Organic solvent-free aqueous solutions of fendiline (hydrochloride) can be prepared by directly dissolving the crystalline solid in aqueous buffers. The solubility of fendiline (hydrochloride) in PBS, pH 7.2, is approximately 0.1 mg/ml. We do not recommend storing the aqueous solution for more than one day. α Fendiline is an 2-adrenergic receptor antagonist (Kd = 2.6 µM) and an L-type calcium channel blocker (IC50 = 17 µM) well-known for its coronary vasodilator effects.1-4 Fendiline has recently been reported to inhibit K-Ras plasma membrane localization (IC50 = 9.64 µM), which prevents K-Ras signal transduction and blocks the proliferation of K-Ras-transformed tumor cells.5 References 1. -
1 the ROLE of SERTONIN and VESICULAR MONOAMINE TRANSPORTERS in the ADVERSE RESPONSES to METHYLENEDIOXYMETHAMPHETAMINE by Lucina
The Role Of Sertonin And Vesicular Monoamine Transporters In The Adverse Responses To Methylenedioxymethamphetamine Item Type text; Electronic Dissertation Authors Lizarraga-Zazueta, Lucina Eridna Publisher The University of Arizona. Rights Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. Download date 24/09/2021 17:03:12 Link to Item http://hdl.handle.net/10150/332686 1 THE ROLE OF SERTONIN AND VESICULAR MONOAMINE TRANSPORTERS IN THE ADVERSE RESPONSES TO METHYLENEDIOXYMETHAMPHETAMINE by Lucina Eridna Lizarraga Zazueta A Dissertation Submitted to the Faculty of the DEPARTMENT OF PHARMACOLOGY AND TOXICOLOGY In Partial Fulfillment of the Requirements For the Degree of DOCTOR OF PHILOSOPHY In the Graduate College at THE UNIVERSITY OF ARIZONA 2014 2 THE UNIVERSITY OF ARIZONA GRADUATE COLLEGE As members of the Dissertation Committee, we certify that we have read the dissertation prepared by Lucina Eridna Lizarraga Zazueta entitled “The Role of Serotonin and Vesicular Monoamine Transporters in the Adverse Responses to Methylenedioxymethamphetamine” and recommend that it be accepted as fulfilling the dissertation requirement for the Degree of Doctor of Philosophy ________________________________________________________________Date: 06/20/2014 Dr. Terrence J. Monks ________________________________________________________________Date: 06/20/2014 Dr. Serrine S. Lau ________________________________________________________________Date: 06/20/2014 Dr. John W. Regan _______________________________________________________________Date: 06/20/2014 Dr. Josephine Lai ________________________________________________________________Date: 06/20/2014 Dr. Stephen Wright Final approval and acceptance of this dissertation is contingent upon the candidate’s submission of the final copies of the dissertation to the Graduate College. -
Pharmacology and Toxicology of Amphetamine and Related Designer Drugs
Pharmacology and Toxicology of Amphetamine and Related Designer Drugs U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES • Public Health Service • Alcohol Drug Abuse and Mental Health Administration Pharmacology and Toxicology of Amphetamine and Related Designer Drugs Editors: Khursheed Asghar, Ph.D. Division of Preclinical Research National Institute on Drug Abuse Errol De Souza, Ph.D. Addiction Research Center National Institute on Drug Abuse NIDA Research Monograph 94 1989 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Alcohol, Drug Abuse, and Mental Health Administration National Institute on Drug Abuse 5600 Fishers Lane Rockville, MD 20857 For sale by the Superintendent of Documents, U.S. Government Printing Office Washington, DC 20402 Pharmacology and Toxicology of Amphetamine and Related Designer Drugs ACKNOWLEDGMENT This monograph is based upon papers and discussion from a technical review on pharmacology and toxicology of amphetamine and related designer drugs that took place on August 2 through 4, 1988, in Bethesda, MD. The review meeting was sponsored by the Biomedical Branch, Division of Preclinical Research, and the Addiction Research Center, National Institute on Drug Abuse. COPYRIGHT STATUS The National Institute on Drug Abuse has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other matieral in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors. -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
Current Research on Methamphetamine-Induced Neurotoxicity: Animal Models of Monoamine Disruption
J Pharmacol Sci 92, 178 – 195 (2003) Journal of Pharmacological Sciences ©2003 The Japanese Pharmacological Society Critical Review Current Research on Methamphetamine-Induced Neurotoxicity: Animal Models of Monoamine Disruption Taizo Kita1,2, George C. Wagner3, and Toshikatsu Nakashima1,* 1Department of Pharmacology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521 2Department of Pharmacology, Daiichi College of Pharmaceutical Sciences, 22-1 Tamagawacho, Minamiku, Fukuoka 815-8511, Japan 3Department of Psychology, Rutgers, The State University, New Brunswick, NJ 08903, USA Received March 6, 2003 Abstract. Methamphetamine (METH)-induced neurotoxicity is characterized by a long-lasting depletion of striatal dopamine (DA) and serotonin as well as damage to striatal dopaminergic and serotonergic nerve terminals. Several hypotheses regarding the mechanism underlying METH- induced neurotoxicity have been proposed. In particular, it is thought that endogenous DA in the striatum may play an important role in mediating METH-induced neuronal damage. This hypo- thesis is based on the observation of free radical formation and oxidative stress produced by auto- oxidation of DA consequent to its displacement from synaptic vesicles to cytoplasm. In addition, METH-induced neurotoxicity may be linked to the glutamate and nitric oxide systems within the striatum. Moreover, using knockout mice lacking the DA transporter, the vesicular monoamine transporter 2, c-fos, or nitric oxide synthetase, it was determined that these factors may be connected in some way to METH-induced neurotoxicity. Finally a role for apoptosis in METH- induced neurotoxicity has also been established including evidence of protection of bcl-2, expres- sion of p53 protein, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), activity of caspase-3. -
Investigator's Brochure SPONSOR Multidisciplinary Association For
Investigator’s Brochure SPONSOR Multidisciplinary Association for Psychedelic Studies (MAPS) 3141 Stevens Creek Blvd #40563 San Jose, CA 95117 PRODUCT 3,4-methylenedioxymethamphetamine (MDMA) DATA CUT-OFF DATE 01 October 2020 VERSION DATE 22 March 2021 EFFECTIVE DATE 31 March 2021 EDITION 13th Edition REPLACES 12th Edition (dated 17 August 2020) MAPS MDMA Investigator’s Brochure U.S. 13th Ed: 22 March 2021 Table of Contents List of Tables .................................................................................................................................. 5 List of Appendix Tables................................................................................................................. 7 List of Figures ................................................................................................................................. 8 List of Abbreviations ..................................................................................................................... 9 1.0 Summary ................................................................................................................................. 11 2.0 Introduction ............................................................................................................................ 13 3.0 Physical, Chemical, and Pharmaceutical Properties and Formulation ............................ 15 4.0 Nonclinical Studies ................................................................................................................. 17 4.1 Nonclinical Pharmacology -
Effect of a Brief Memory Updating Intervention On
1 1 2 PI Name: Michael E. Saladin, PhD 3 4 Study Title: Reducing Smoking Cue Reactivity and Behavior via Retrieval-Extinction Mechanism 5 A. Specific Aims 6 The goal of the study will be to adopt many of the procedures and parameters of retrieval- 7 extinction training in an attempt to demonstrate enduring reductions in craving and cue-reactivity 8 among cigarette smokers. The study will conduct an exploratory analysis of the intervention’s effects on 9 substance use (i.e., smoking behavior). This exploratory study will investigate a novel behavioral 10 strategy for altering important memory processes that underlie human smoking-related nicotine 11 addiction. This strategy represents a paradigm shift in that it employs established cue exposure 12 procedures to putatively update1 smoking–related memory with information that will suppress 13 responding to smoking cues. The goal here is to alter existing nicotine-related memory directly rather 14 than rely exclusively on the establishment of an inhibitory extinction process2-6 via traditional cue 15 exposure therapy, which is known to be vulnerable to spontaneous recovery, renewal, and 16 reinstatement7,8. The proposed study will also be innovative and novel because, unlike the Xue et al. 17 2012 study, we will preliminarily assess, over the course of a 1-month follow-up period, the effects of 18 retrieval-extinction training on the smoking behavior of smokers who have made a cessation attempt. 19 20 B. Background and Significance 21 Smoking occurs in approximately 21% of the US population, is responsible for an annual 22 mortality rate of approximately 438,000 citizens, and has an associated healthcare economic burden of 23 $167 billion9. -
WO 2013/061161 A2 2 May 2013 (02.05.2013) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2013/061161 A2 2 May 2013 (02.05.2013) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 31/337 (2006.01) A61K 31/48 (2006.01) kind of national protection available): AE, AG, AL, AM, A61K 31/395 (2006.01) A61K 31/51 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, A61K 31/4174 (2006.01) A61K 31/549 (2006.01) BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, A61K 31/428 (2006.01) A61K 31/663 (2006.01) DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, (21) International Application Number: KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, PCT/IB20 12/002768 ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, (22) International Filing Date: NO, NZ, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, 25 October 2012 (25.10.2012) RW, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, (25) Filing Language: English ZM, ZW. (26) Publication Language: English (84) Designated States (unless otherwise indicated, for every (30) Priority Data: kind of regional protection available): ARIPO (BW, GH, 61/552,922 28 October 201 1 (28. -
The Role of Habituation in Social Fear by Suzanne N. Avery Dissertation
Slow to Warm Up: The Role of Habituation in Social Fear By Suzanne N. Avery Dissertation Submitted to the Faculty of the Graduate School of Vanderbilt University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY in Neuroscience August, 2015 Nashville, Tennessee Approved: David Zald, Ph.D. Bunmi Olatunji, Ph.D. Brandon Ally, Ph.D. Jennifer Blackford, Ph.D. Copyright © 2015 by Suzanne N. Avery All Rights Reserved ii To my husband, Stacy, for his unending support, and my daughter, Sophie, for whom I do everything iii ACKNOWLEDGMENTS I would first and foremost like to thank my advisor, Dr. Jennifer Blackford, who is a truly exceptional scientist, teacher and mentor. She has encouraged me to pursue every opportunity for scientific achievement and has mentored me closely through each step. Her enthusiasm to help me become an excellent scientist and her generosity with her time and effort have made my graduate training an incredible experience. She has an incredible passion for science and possesses a brilliant combination of curiosity, creativity, motivation, intelligence and passion that inspires all of those who have the pleasure to work with her. I am eternally grateful for your mentorship—thank you is not enough. I would also like to thank the current and former members of the Blackford lab, including Jacqueline Clauss, Ross VanDerKlok, and Brittany Matthews, whose assistance and encouragement have made this work possible. My gratitude goes out to my dissertation committee, who have provided invaluable feedback and whose suggestions have significantly improved this project. Thank you for your insights and help Dr.