DOCSLIB.ORG

Enduring Changes in Brain and Behavior Produced by Chronic Amphetamine Administration: a Review and Evaluation of Animal Models of Amphetamine Psychosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Enduring Changes in Brain and Behavior Produced by Chronic Amphetamine Administration: a Review and Evaluation of Animal Models of Amphetamine Psychosis Brain Research Reviews, 11 (1986) 157-198 157 Elsevier BRR 90048 Enduring Changes in Brain and Behavior Produced by Chronic Amphetamine Administration: A Review and Evaluation of Animal Models of Amphetamine Psychosis TERRY E. ROBINSON and JILL B. BECKER Department of Psychology and Neuroscience Laboratory Building, The University of Michigan, Ann Arbor, M148104-1687 (U.S.A.) (Accepted December 31st, 1985) Key words: amphetamine -- sensitization -- reverse tolerance -- dopamine -- catecholamine -- schizophrenia -- amphetamine psychosis -- animal model -- striatum-- stress-- sex difference -- conditioning-- neurotoxicity -- stereotypy -- autoreceptor CONTENTS 1. Introduction ............................................................................................................................................ 158 2. The effects of continuous amphetamine administration on brain and behavior (amphetamine neurotoxicity) ..................... 159 3. The behavioral consequences of repeated intermittent amphetamine administration (behavioral sensitization) ................. 160 3 1. The major characteristics of behavioral sensitization .................................................................................... 161 3.1.1. Behavior .................................................................................................................................. 161 3.1.2. Injection paradigm ..................................................................................................................... 163 3.1.3. Sex differences ........................................................................................................................... 163 3.1.4. Summary .................................................................. "................................................................ 164 4. Behavioral sensitization and amphetamine neurotoxicity as animal models of amphetamine psychosis ............................. 164 5. The biological basis of behavioral sensitization .................................................................................................. 167 5 1. Drug dispositional/peripheral hypotheses .................................................................................................. 167 5_2 Drug-environment conditioning hypotheses ............................................................................................... 167 5.3. Neural hypotheses ............................................................................................................................... 169 5.3.1. The nigrostriatal dopamine system .................................................................................................. 169 5.3_1.1. Evidence for postsynaptic changes ....................................................................................... 169 5.3.1_2. Evidence forpresynapticchanges ........................................................................................ 172 5.3.1.3_ Dopamine autoreceptor subsensitivity ................................................................................. 176 5.3.1.4. Other hypotheses ............................................................................................................ 179 5.3.2. The mesolimbic and mesocortical dopamine systems ........................................................................... 179 5.3.3. Other neurotransmitter systems ..................................................................................................... 182 5.3.3 1. Opiate peptide-dopamine interactions ................................................................................ 182 5.3.3_2. Norepinephrine .............................................................................................................. 182 5.3.3.3. Serotonin ...................................................................................................................... 183 5.3.3.4. Amino acids ................................................................................................................. 183 5.4. The neural basis of behavioral sensitization: conclusions and a hypothesis .......................................................... 184 6. Generalizability of sensitization ..................................................................................................................... 185 6.1. Stimulants and stress ............................................................................................................................ 185 6.2. Sex differences, stimulants and stress ........................................................................................................ 186 7. Conclusions ............................................................................................................................................. 187 Correspondence." T.E. Robinson, The University of Michigan, Neuroscience Laboratory Building, 1103 E. Huron St., Ann Arbor, MI 48104-1687, U.S.A. 0165-0173/86/$03.50 © 1986 Elsevier Science Publishers B.V. (Biomedical Division) 158 8. Summary ................................................................................................................................................ 188 Acknowledgements ........................................................................................................................................ 188 References ................................................................................................................................................... 189 1. INTRODUCTION nence 248'3°2 (cf. ref. 99). There are also anecdotal re- ports that 'physical or psychological stress' can pre- The use of stimulant drugs to decrease fatigue and cipitate a psychotic episode in 20-25% of former to heighten physical and mental abilities began when AMPH addicts 3°2'3°3. This suggests that chronic people first identified plants with these properties. AMPH use produces a very long-lasting change in For example, in ancient China herbal teas were some neural system(s) involved in the psychotomi- brewed with plants containing ephedrine, and coco metic effects of AMPH. leaves, the source of cocaine, were chewed in South These clinical observations generated considera- America by the ancestors of the Incas (see ref. 12 for ble interest in the effects of chronic AMPH adminis- an excellent historical review of central nervous sys- tration on brain and behavior in non-human animals, tem stimulants). Today, stimulant drugs such as the and in the development of animal models of AMPH- amphetamines remain among the most widely used induced psychosis. There are now many studies and abused of the many psychoactive compounds showing that chronic AMPH administration has en- available. Although at one time amphetamine during consequences for behavior and brain function (AMPH) was prescribed in great numbers, for exam- in non-human animals, and one purpose of this paper ple as an anorexic in the treatment of obesity, its is to review this literature. However, even a cursory medical use has been greatly curtailed in recent examination of the literature reveals that at least two years. AMPH is now usually prescribed only for the different paradigms have been used to study the ef- treatment of narcolepsy and childhood hyperkinesis. fects of chronic AMPH administration. With one Nevertheless, illicit AMPH is still widely available paradigm, elevated brain concentrations of AMPH and extensively used for its ability to decrease fa- are maintained for a few days, either by the continu- tigue, elevate mood and produce euphoria 96 (AMPH ous administration of AMPH or by multiple repeated will be used to refer collectively to D-, L-, DL- and injections of high doses. The other paradigm involves meth-amphetamine). the repeated intermittent administration of AMPH, However, it is not fully appreciated that AMPH is usually by discrete daily injections of relatively low also a potent psychotomimetic. In some schizophren- doses. Since it will become obvious that these two ics it can rapidly intensify psychotic symptoms, and if paradigms produce different effects on brain and be- a patient is in remission AMPH may precipitate a havior, studies relevant to each will be reviewed sep- psychotic episode 265,275. In fact, an AMPH-induced arately. exacerbation of symptoms in medicated schizophren- Continuous AMPH administration produces a syn- ics is predictive of relapse following neuroleptic with- drome that will be called 'AMPH neurotoxicity'. The drawal 3°5. Perhaps the most dramatic effect of literature on AMPH neurotoxicity has been re- AMPH has been described in people who chronically viewed recently (e.g. ref. 81), and therefore will be use the drug. It has been well documented that non- only briefly summarized to provide a comparison psychotic individuals who repeatedly use AMPH with the effects of repeated intermittent AMPH ad- sometimes develop a psychosis that is very similar to ministration. The major portion of this paper will fo- paranoid schizophrenia ~s,32° (for reviews of AMPH cus on a phenomenon that will be called 'behavioral psychosis see refs. 124, 213, 264, 268, 275). This sensitization', which is produced by repeated inter- AMPH-induced psychosis usually dissipates upon mittent AMPH administration. In particular, an in- withdrawal from the drug, but former AMPH addicts depth and critical analysis of hypotheses concerning are reported to remain hypersensitive to the psycho- the biological basis of behavioral sensitization is pre- tomimetic
Load more

Recommended publications
  • Tolerance and Dependence
    Tolerance and Dependence Drug Tolerance is a decrease in the effect of a drug as a consequence of repeated exposure. • Change over repeated exposures. • Different effects may show different tolerance. • Tolerance is reversible. Mechanisms of Tolerance • Pharmacokinetic Tolerance • Enzyme Induction Effects. • Pharmacodynamic Tolerance • NT depletion • Receptor Plasticity 1 Receptor Plasticity and Tolerance • Drugs that are NT agonists can cause receptor downregulation. • Drugs that are NT antagonists can cause receptor upregulation. Pharmacodynamic drug tolerance can also affect “normal” synaptic transmission. • Serious side-effect of drug use. Mechanisms of tolerance continued… Learned Tolerance - Learned behaviors compensate for drug effects. • Practice effects. • Reward and punishment . Context-Specific Tolerance • Stimuli in the environment (context) become able to counteract the effects of a drug. Pavlovian Conditioning • A neutral stimulus paired with a biologically relevant stimulus becomes able to elicit a response. Siegel et al. (1982) - Demonstrated that drug tolerance can be conditioned. 2 Group Control 15 injections of saline in distinctive room. High dose of heroin in distinctive room on Day 16. • Results: 96% died of overdose. Group Same 15 injections of heroin in distinctive room. Hig h dose o f hero in in dis tincti ve room on D ay 16 . • Results: 32% died of overdose. Group Different 15 injections of heroin in distinctive room. High dose of heroin in new room on Day 16. • Results: 64% died of overdose. Siegel’s Theory: • When an environment consistently predicts drug administration... • … the environment begins to elicit a “compensatory” response that is opposite to the drug’s effect. • The compensatory response counteracts the drug’s effect.
    [Show full text]
  • AND DRUG' ABUSE' ( , \ I ., : for VOLUNTEER .AFTERCARE OFFICERS
    =£q, G& ~. ~I o II g ~ L>- ".,-~..- ". 'PR'OBATIQN AND AFTERCA'RE SERVICE " rI ! ,~ i I!' 0 i! ,1 u I', :( ~ II' 1 r :.:" I I) 'tbLLECTED ,READINGS ,~ ~ - '., ,\ ON It, DR!J.GS ·AND DRUG' ABUSE' ( , \ i ., : FOR VOLUNTEER .AFTERCARE OFFICERS. ri ll, "' , 'I: o '.> .. , 4 . , . I:o..-__________:i-.._---... __ ~~ ___~;L __~ ______ fF PROBATION AND AFTERCARE SERVICE COLLECTED READUNGS ON DRUGS AND DRUG ABUSE FOR VOLUNTEER AFTERCARE OFFICERS 1977 a If' t «(, CONTENTS ARTICLE PAGE PART I - THE DRUG SCENE Speech by Dr Goh Keng Swee, Deputy Prime Minister and Minister of Defence, at the Launching of the NADAC Month at the National Theatre Or! Wedr!e~dev, 4th August 1976. 1 II Speech by Mr Chua Sian Chin, Minister for Home Affairs and Education at the Opening Ceremony of the First Meeting of ASEAN Drug Experts at the Crystal Ballroom, Hyatt Hotel, on Tuesday, 26th October 1976. 6 PART II - PREVENTIVE EDUCATION III The Objectives of Anti-Drug Abuse Education by Dr Tow Siang Hwa, Past President, Singapore Anti-Narcotics Association 8 .. PART III - DRUGS AND THEIR EFFECTS IV CommonlY Abused Drugs by Dr Yeow Teow Seng, Associate Profassor oi Pharmacology, University of Singapore 12 V The Non-Medical Uses of Dependence-Producing Drugs by Dr Leong Hon Koon 18 VI Psychiatric Aspects of Drug Abuse by Dr Paul W Ngui, Consultant Psychlatrist 23 VII Sad End to All Drug Trips by Dr Chao Tzu Cheng, Senior Forensic Pathologist, Ministry of Health 27 PART IV - SOCIAL CONSIDERATIONS OF DRUG ABUSE VIII Patterns & Social Consequences of Drug Abuse & the Rehabilitation of Drug Addict by K V Veloo, Chief Probation & Aftercare Officer 29 IX Social Factors of Drug Abuse by K V Veloo, Chief Probation & Aftercare Officer 34 f X Some Causes of Adolescent Problems , by S Vasoo, Deputy Director, Singapore Council of Social Service 39 " ,.
    [Show full text]
  • Amphetamine Sensitization Alters Hippocampal Neuronal Morphology and Memory and Learning Behaviors
    Molecular Psychiatry https://doi.org/10.1038/s41380-020-0809-2 ARTICLE Amphetamine sensitization alters hippocampal neuronal morphology and memory and learning behaviors 1,2,5 1,2 1 Luis Enrique Arroyo-García ● Hiram Tendilla-Beltrán ● Rubén Antonio Vázquez-Roque ● 1 3 3 3 1 Erick Ernesto Jurado-Tapia ● Alfonso Díaz ● Patricia Aguilar-Alonso ● Eduardo Brambila ● Eduardo Monjaraz ● 2 4 1 Fidel De La Cruz ● Antonio Rodríguez-Moreno ● Gonzalo Flores Received: 12 November 2019 / Revised: 29 May 2020 / Accepted: 3 June 2020 © The Author(s), under exclusive licence to Springer Nature Limited 2020 Abstract It is known that continuous abuse of amphetamine (AMPH) results in alterations in neuronal structure and cognitive behaviors related to the reward system. However, the impact of AMPH abuse on the hippocampus remains unknown. The aim of this study was to determine the damage caused by AMPH in the hippocampus in an addiction model. We reproduced the AMPH sensitization model proposed by Robinson et al. in 1997 and performed the novel object recognition test (NORt) to evaluate learning and memory behaviors. After the NORt, we performed Golgi–Cox staining, a 1234567890();,: 1234567890();,: stereological cell count, immunohistochemistry to determine the presence of GFAP, CASP3, and MT-III, and evaluated oxidative stress in the hippocampus. We found that AMPH treatment generates impairment in short- and long-term memories and a decrease in neuronal density in the CA1 region of the hippocampus. The morphological test showed an increase in the total dendritic length, but a decrease in the number of mature spines in the CA1 region. GFAP labeling increased in the CA1 region and MT-III increased in the CA1 and CA3 regions.
    [Show full text]
  • How Psychoactive Drugs Affect Us
    HOW PSYCHOACTIVE DRUGS AFFECT US Part II 7th February 2014 Ms. Cathy Ngarachu Physiological Responses to Drugs • Determines how drugs affect people and why it is difficult to control their levels of use. • They include: • Tolerance to Drug • Tissue Dependence • Psychological Dependence & Reward-reinforcing action of drugs • Withdrawal Tolerance • Results from the body’s attempt to eliminate a drug that it treats as a toxin • With continued drug use the body tries to neutralize the toxic effects by: • Requiring larger amounts of the drugs to achieve the original effects • Degree of effects depend on the : • Amount used • Duration of use • Frequency of use • Individual’s chemistry • State of mind Kinds of Tolerance • Dispositional Tolerance • Speeds up the metabolism to handle the drug in order to eliminate it • Example: Increases the amount of cytocells and mitochondria in the liver to neutralize the drug….. So it will take more of the drug to achieve the same level of intoxication Kinds of Tolerance • Pharmacodynamic Tolerance • Results from the desensitization of nerve cells to the action of the drug • Ex. The nerve cells become less sensitive and begin producing an antidote or antagonist to the drug, ie. The brain will generate more opiod receptor sites. Kinds of Tolerance • Behavioral Tolerance: • Brain adjustments that affect behavior • Someone who is high may make himself appear sober when threatened, then revert back to the high state • Reverse Tolerance • Person has greater sensitivity to the drug, after prolong use, and the body’s ability to metabolize the drug decreases. • Ex. A person who has drunk a 12-pack of beer daily for ten years, may find themselves drinking 3-4 beers to achieve the effect due to tissue damage of the liver and kidneys.
    [Show full text]
  • Neurobiological and Neurobehavioral Mechanisms of Chronic Alcohol Drinking
    Neurobiological and Neurobehavioral Mechanisms of Chronic Alcohol Drinking Neurobiological and Neurobehavioral Mechanisms of Chronic Alcohol Drinking Alcoholism comprises a set of complex behaviors seeking behaviors, have been developed. These in which an individual becomes increasingly models, which remain an integral part of the preoccupied with obtaining alcohol. These study of alcoholism, include animals that pref- behaviors ultimately lead to a loss of control over erentially drink solutions containing alcohol, consumption of the drug and to the development animals that self-administer alcohol during of tolerance, dependence, and impaired social and withdrawal, animals with a history of dependence occupational functioning. that self-administer alcohol, and animals that self- administer alcohol after a period of abstinence Although valuable information regarding toler- from the drug. Genetic models for alcoholism ance and dependence has been, and continues to also exist and include animals that have been bred be, gathered through human studies, much of the selectively for high alcohol consumption. Studies detailed understanding of the impact of exposure using such models are uncovering the systemic, to alcohol on behavior and on the biological cellular, and molecular neurobiological mech- mechanisms underlying those behaviors has been anisms that appear to contribute to chronic obtained through the use of animal models for alcohol consumption. The challenge of current alcoholism and a variety of in vitro, or cellular, and future studies is to understand which specific systems. Through the use of cellular systems and cellular and subcellular systems undergo mole- animal models, researchers can control the genetic cular changes to influence tolerance and depen- background and experimental conditions under dence in motivational systems that lead to which a specific alcohol-related behavior or chronic drinking.
    [Show full text]
  • (19) United States (12) Patent Application Publication (10) Pub
    US 20130289061A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0289061 A1 Bhide et al. (43) Pub. Date: Oct. 31, 2013 (54) METHODS AND COMPOSITIONS TO Publication Classi?cation PREVENT ADDICTION (51) Int. Cl. (71) Applicant: The General Hospital Corporation, A61K 31/485 (2006-01) Boston’ MA (Us) A61K 31/4458 (2006.01) (52) U.S. Cl. (72) Inventors: Pradeep G. Bhide; Peabody, MA (US); CPC """"" " A61K31/485 (201301); ‘4161223011? Jmm‘“ Zhu’ Ansm’ MA. (Us); USPC ......... .. 514/282; 514/317; 514/654; 514/618; Thomas J. Spencer; Carhsle; MA (US); 514/279 Joseph Biederman; Brookline; MA (Us) (57) ABSTRACT Disclosed herein is a method of reducing or preventing the development of aversion to a CNS stimulant in a subject (21) App1_ NO_; 13/924,815 comprising; administering a therapeutic amount of the neu rological stimulant and administering an antagonist of the kappa opioid receptor; to thereby reduce or prevent the devel - . opment of aversion to the CNS stimulant in the subject. Also (22) Flled' Jun‘ 24’ 2013 disclosed is a method of reducing or preventing the develop ment of addiction to a CNS stimulant in a subj ect; comprising; _ _ administering the CNS stimulant and administering a mu Related U‘s‘ Apphcatlon Data opioid receptor antagonist to thereby reduce or prevent the (63) Continuation of application NO 13/389,959, ?led on development of addiction to the CNS stimulant in the subject. Apt 27’ 2012’ ?led as application NO_ PCT/US2010/ Also disclosed are pharmaceutical compositions comprising 045486 on Aug' 13 2010' a central nervous system stimulant and an opioid receptor ’ antagonist.
    [Show full text]
  • Neuroplasticity in the Mesolimbic System Induced by Sexual Experience and Subsequent Reward Abstinence
    Western University Scholarship@Western Electronic Thesis and Dissertation Repository 6-21-2012 12:00 AM Neuroplasticity in the Mesolimbic System Induced by Sexual Experience and Subsequent Reward Abstinence Kyle Pitchers The University of Western Ontario Supervisor Lique M. Coolen The University of Western Ontario Graduate Program in Anatomy and Cell Biology A thesis submitted in partial fulfillment of the equirr ements for the degree in Doctor of Philosophy © Kyle Pitchers 2012 Follow this and additional works at: https://ir.lib.uwo.ca/etd Recommended Citation Pitchers, Kyle, "Neuroplasticity in the Mesolimbic System Induced by Sexual Experience and Subsequent Reward Abstinence" (2012). Electronic Thesis and Dissertation Repository. 592. https://ir.lib.uwo.ca/etd/592 This Dissertation/Thesis is brought to you for free and open access by Scholarship@Western. It has been accepted for inclusion in Electronic Thesis and Dissertation Repository by an authorized administrator of Scholarship@Western. For more information, please contact [email protected]. NEUROPLASTICITY IN THE MESOLIMBIC SYSTEM INDUCED BY SEXUAL EXPERIENCE AND SUBSEQUENT REWARD ABSTINENCE (Spine Title: Sex, Drugs and Neuroplasticity) (Thesis Format: Integrated Article) By Kyle Kevin Pitchers Graduate Program in Anatomy and Cell Biology A thesis submitted in partial fulfillment of the requirements for degree of Doctor of Philosophy The School of Graduate and Postdoctoral Studies The University of Western Ontario London, Ontario, Canada © Kyle K. Pitchers, 2012 THE UNIVERSITY
    [Show full text]
  • Selective Serotonin Reuptake Inhibitors, Fluoxetine and Paroxetine, Attenuate the Expression of the Established Behavioral Sensitization Induced by Methamphetamine
    Neuropsychopharmacology (2007) 32, 658–664 & 2007 Nature Publishing Group All rights reserved 0893-133X/07 $30.00 www.neuropsychopharmacology.org Selective Serotonin Reuptake Inhibitors, Fluoxetine and Paroxetine, Attenuate the Expression of the Established Behavioral Sensitization Induced by Methamphetamine 1 1 1 1 1 ,1 Yujiro Kaneko , Atsushi Kashiwa , Takashi Ito , Sumikazu Ishii , Asami Umino and Toru Nishikawa* 1 Section of Psychiatry and Behavioral Sciences, Tokyo Medical and Dental University Graduate School, Yushima, Bunkyo-ku, Tokyo, Japan To obtain an insight into the development of a new pharmacotherapy that prevents the treatment-resistant relapse of psychostimulant- induced psychosis and schizophrenia, we have investigated in the mouse the effects of selective serotonin reuptake inhibitors (SSRI), fluoxetine (FLX) and paroxetine (PRX), on the established sensitization induced by methamphetamine (MAP), a model of the relapse of these psychoses, because the modifications of the brain serotonergic transmission have been reported to antagonize the sensitization phenomenon. In agreement with previous reports, repeated MAP treatment (1.0 mg/kg a day, subcutaneously (s.c.)) for 10 days induced a long-lasting enhancement of the increasing effects of a challenge dose of MAP (0.24 mg/kg, s.c.) on motor activity on day 12 or 29 of withdrawal. The daily injection of FLX (10 mg/kg, s.c.) or PRX (8 mg/kg, s.c.) from 12 to 16 days of withdrawal of repeated MAP administration markedly attenuated the ability of the MAP pretreatment to augment the motor responses to the challenge dose of the stimulant 13 days after the SSRI injection. The repeated treatment with FLX or PRX alone failed to affect the motor stimulation following the challenge of saline and MAP 13 days later.
    [Show full text]
  • Comparison Between Two Methodological Paradigms of Conditioned Place Preference with Methlyphenidate
    East Tennessee State University Digital Commons @ East Tennessee State University Undergraduate Honors Theses Student Works 12-2013 Comparison between Two Methodological Paradigms of Conditioned Place Preference with Methlyphenidate. Bryce D. Watson East Tennessee State University Follow this and additional works at: https://dc.etsu.edu/honors Part of the Psychiatry and Psychology Commons Recommended Citation Watson, Bryce D., "Comparison between Two Methodological Paradigms of Conditioned Place Preference with Methlyphenidate." (2013). Undergraduate Honors Theses. Paper 89. https://dc.etsu.edu/honors/89 This Honors Thesis - Open Access is brought to you for free and open access by the Student Works at Digital Commons @ East Tennessee State University. It has been accepted for inclusion in Undergraduate Honors Theses by an authorized administrator of Digital Commons @ East Tennessee State University. For more information, please contact [email protected]. Watson 1 Comparison between Two Methodological Paradigms of Conditioned Place Preference with Methlyphenidate By Bryce Watson The Honors College Honors in Discipline Program East Tennessee State University Department of Psychology December 9, 2013 Russell Brown, Faculty Mentor David Harker, Faculty Reader Eric Sellers, Faculty Reader Watson 2 Abstract The aim of this thesis is to examine the mechanisms of Methylphenidate (MPH) on Conditioned Place Preference (CPP), a behavioral test of reward. The psychostimulant MPH is therapeutically used in the treatment of ADHD, but has been implicated in many pharmacological actions related to drug addiction and is considered to have abuse potential. Past work in our lab and others have shown substantial sex-differences in the neuropharmacological profile of MPH. Here a discussion of the relevant mechanisms of action of MPH and its relationship to neurotrophins and CPP are reviewed.
    [Show full text]
  • D, Dopamine Receptor Activation Is Necessary for the Induction of Sensitization by Amphetamine in the Ventral Tegmental Area
    The Journal of Neuroscience, April 1, 1996, 76(7):241 l-2420 D, Dopamine Receptor Activation Is Necessary for the Induction of Sensitization by Amphetamine in the Ventral Tegmental Area Paul Vezina Department of Psychiatry, The University of Chicago, Chicago, Illinois 6063 7 Repeated intermittent exposure to amphetamine produces injections of amphetamine. In the second experiment, locomo- long-term enhancements in the ability of this drug to produce tor sensitization induced by infusion of amphetamine into the locomotion and increase extracellular dopamine (DA) in the ventral tegmental area (WA) was blocked when these injections nucleus accumbens (NAcc). Three experiments were con- were preceded by systemic injections of SCH23390. Finally, in ducted to evaluate the role played by D, DA receptors in the experiment three, co-injecting SCH23390, but not its inactive production of these changes in response to amphetamine. Rats enantiomer, with amphetamine into the VTA during preexpo- were preexposed to amphetamine, alone or with a DA receptor sure prevented sensitization of the NAcc DA response to this antagonist, and tested for sensitization l-3 weeks after the last drug. These results indicate that while D, DA receptor activa- drug injection. On the test for sensitization, locomotor (experi- tion is not necessary for the induction of locomotor sensitiza- ments 1 and 2) and NAcc DA (experiment 3) responses of the tion to amphetamine, D, DA receptors located in the VTA play animals to a systemic amphetamine injection were assessed. In a critical role in the development of sensitized locomotor and the first experiment, systemic injections of the D, DA receptor NAcc DA response to this drug.
    [Show full text]
  • ASAM National Practice Guideline for the Treatment of Opioid Use Disorder: 2020 Focused Update
    The ASAM NATIONAL The ASAM National Practice Guideline 2020 Focused Update Guideline 2020 Focused National Practice The ASAM PRACTICE GUIDELINE For the Treatment of Opioid Use Disorder 2020 Focused Update Adopted by the ASAM Board of Directors December 18, 2019. © Copyright 2020. American Society of Addiction Medicine, Inc. All rights reserved. Permission to make digital or hard copies of this work for personal or classroom use is granted without fee provided that copies are not made or distributed for commercial, advertising or promotional purposes, and that copies bear this notice and the full citation on the fi rst page. Republication, systematic reproduction, posting in electronic form on servers, redistribution to lists, or other uses of this material, require prior specifi c written permission or license from the Society. American Society of Addiction Medicine 11400 Rockville Pike, Suite 200 Rockville, MD 20852 Phone: (301) 656-3920 Fax (301) 656-3815 E-mail: [email protected] www.asam.org CLINICAL PRACTICE GUIDELINE The ASAM National Practice Guideline for the Treatment of Opioid Use Disorder: 2020 Focused Update 2020 Focused Update Guideline Committee members Kyle Kampman, MD, Chair (alpha order): Daniel Langleben, MD Chinazo Cunningham, MD, MS, FASAM Ben Nordstrom, MD, PhD Mark J. Edlund, MD, PhD David Oslin, MD Marc Fishman, MD, DFASAM George Woody, MD Adam J. Gordon, MD, MPH, FACP, DFASAM Tricia Wright, MD, MS Hendre´e E. Jones, PhD Stephen Wyatt, DO Kyle M. Kampman, MD, FASAM, Chair 2015 ASAM Quality Improvement Council (alpha order): Daniel Langleben, MD John Femino, MD, FASAM Marjorie Meyer, MD Margaret Jarvis, MD, FASAM, Chair Sandra Springer, MD, FASAM Margaret Kotz, DO, FASAM George Woody, MD Sandrine Pirard, MD, MPH, PhD Tricia E.
    [Show full text]
  • Compositions and Methods for Selective Delivery of Oligonucleotide Molecules to Specific Neuron Types
    (19) TZZ ¥Z_T (11) EP 2 380 595 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 26.10.2011 Bulletin 2011/43 A61K 47/48 (2006.01) C12N 15/11 (2006.01) A61P 25/00 (2006.01) A61K 49/00 (2006.01) (2006.01) (21) Application number: 10382087.4 A61K 51/00 (22) Date of filing: 19.04.2010 (84) Designated Contracting States: • Alvarado Urbina, Gabriel AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Nepean Ontario K2G 4Z1 (CA) HR HU IE IS IT LI LT LU LV MC MK MT NL NO PL • Bortolozzi Biassoni, Analia Alejandra PT RO SE SI SK SM TR E-08036, Barcelona (ES) Designated Extension States: • Artigas Perez, Francesc AL BA ME RS E-08036, Barcelona (ES) • Vila Bover, Miquel (71) Applicant: Nlife Therapeutics S.L. 15006 La Coruna (ES) E-08035, Barcelona (ES) (72) Inventors: (74) Representative: ABG Patentes, S.L. • Montefeltro, Andrés Pablo Avenida de Burgos 16D E-08014, Barcelon (ES) Edificio Euromor 28036 Madrid (ES) (54) Compositions and methods for selective delivery of oligonucleotide molecules to specific neuron types (57) The invention provides a conjugate comprising nucleuc acid toi cell of interests and thus, for the treat- (i) a nucleic acid which is complementary to a target nu- ment of diseases which require a down-regulation of the cleic acid sequence and which expression prevents or protein encoded by the target nucleic acid as well as for reduces expression of the target nucleic acid and (ii) a the delivery of contrast agents to the cells for diagnostic selectivity agent which is capable of binding with high purposes.
    [Show full text]