Cerebellar Toxicity of Phencyclidine
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Hallucinogens - LSD, Peyote, Psilocybin, and PCP
Information for Behavioral Health Providers in Primary Care Hallucinogens - LSD, Peyote, Psilocybin, and PCP What are Hallucinogens? Hallucinogenic compounds found in some plants and mushrooms (or their extracts) have been used— mostly during religious rituals—for centuries. Almost all hallucinogens contain nitrogen and are classified as alkaloids. Many hallucinogens have chemical structures similar to those of natural neurotransmitters (e.g., acetylcholine-, serotonin-, or catecholamine-like). While the exact mechanisms by which hallucinogens exert their effects remain unclear, research suggests that these drugs work, at least partially, by temporarily interfering with neurotransmitter action or by binding to their receptor sites. This InfoFacts will discuss four common types of hallucinogens: LSD (d-lysergic acid diethylamide) is one of the most potent mood-changing chemicals. It was discovered in 1938 and is manufactured from lysergic acid, which is found in ergot, a fungus that grows on rye and other grains. Peyote is a small, spineless cactus in which the principal active ingredient is mescaline. This plant has been used by natives in northern Mexico and the southwestern United States as a part of religious ceremonies. Mescaline can also be produced through chemical synthesis. Psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine) is obtained from certain types of mushrooms that are indigenous to tropical and subtropical regions of South America, Mexico, and the United States. These mushrooms typically contain less than 0.5 percent psilocybin plus trace amounts of psilocin, another hallucinogenic substance. PCP (phencyclidine) was developed in the 1950s as an intravenous anesthetic. Its use has since been discontinued due to serious adverse effects. How Are Hallucinogens Abused? The very same characteristics that led to the incorporation of hallucinogens into ritualistic or spiritual traditions have also led to their propagation as drugs of abuse. -
Ie-O-JY -CH2 S (56) References Cited Wherein N Is 0 to 6, X" and Y Are Independently H, Cl, F, CH, CH, CH, CH, OCH, OH, CF, OCF, NO, U.S
US005574060A United States Patent (19) 11) Patent Number: 5,574,060 Rothman et al. (45) Date of Patent: Nov. 12, 1996 54 SELECTIVE INHIBITORS OF BIOGENIC "Hydrindene Derivatives as Potential Oral Hypoglycemic AMINE TRANSPORTERS Agents: N-Alkyl 1,2,3,3a,4,8b-Hexahydroindeno1,2-b) pyrroles', De et al., Journal of Pharmaceutical Sciences, vol. (75) Inventors: Richard Rothman, Silver Spring, Md.; 62, No. 8, Aug. 1973, pp. 1363-1364. Frank J. Carroll, Durham, N.C.; Bruce Blough, Raleigh, N.C.; Samuel (List continued on next page.) W. Mascarella, Hillsborough, N.C. Primary Examiner-Mark L. Berch (73) Assignees: The United States of America as Attorney, Agent, or Firm-Morgan & Finnegan LLP represented by the Department of 57) ABSTRACT Health and Human Services, Washington, D.C.; Office of Technology The present invention provides a compound having the Transfer, Bethesda, Md.; Research Structure: Triangle Institue, Research Triangle Park, N.C. (21) Appl. No.: 203,222 22 Filed: Feb. 28, 1994 Related U.S. Application Data H 63 Continuation-in-part of Ser. No. 105,747, Aug. 12, 1993, abandoned. wherein X, Y, and Z are independently H, Cl, Br, F, OCH, I, or an alkyl group having 1 to 6 carbon atoms; and R is (51) Int. Cl." .......................... A61K 31/40; A61K 31/47; C07D 403/06; C07D 471/08 X (52) U.S. Cl. ............................ 514/411; 546/94; 546/146; 54.6/150; 548/427: 548/428 58) Field of Search .............................. 548/427; 514/411 -ie-O-JY -CH2 S (56) References Cited wherein n is 0 to 6, X" and Y are independently H, Cl, F, CH, CH, CH, CH, OCH, OH, CF, OCF, NO, U.S. -
A Role for Sigma Receptors in Stimulant Self Administration and Addiction
Pharmaceuticals 2011, 4, 880-914; doi:10.3390/ph4060880 OPEN ACCESS pharmaceuticals ISSN 1424-8247 www.mdpi.com/journal/pharmaceuticals Review A Role for Sigma Receptors in Stimulant Self Administration and Addiction Jonathan L. Katz *, Tsung-Ping Su, Takato Hiranita, Teruo Hayashi, Gianluigi Tanda, Theresa Kopajtic and Shang-Yi Tsai Psychobiology and Cellular Pathobiology Sections, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Department of Health and Human Services, Baltimore, MD, 21224, USA * Author to whom correspondence should be addressed; E-Mail: [email protected]. Received: 16 May 2011; in revised form: 11 June 2011 / Accepted: 13 June 2011 / Published: 17 June 2011 Abstract: Sigma1 receptors (σ1Rs) represent a structurally unique class of intracellular proteins that function as chaperones. σ1Rs translocate from the mitochondria-associated membrane to the cell nucleus or cell membrane, and through protein-protein interactions influence several targets, including ion channels, G-protein-coupled receptors, lipids, and other signaling proteins. Several studies have demonstrated that σR antagonists block stimulant-induced behavioral effects, including ambulatory activity, sensitization, and acute toxicities. Curiously, the effects of stimulants have been blocked by σR antagonists tested under place-conditioning but not self-administration procedures, indicating fundamental differences in the mechanisms underlying these two effects. The self administration of σR agonists has been found in subjects previously trained to self administer cocaine. The reinforcing effects of the σR agonists were blocked by σR antagonists. Additionally, σR agonists were found to increase dopamine concentrations in the nucleus accumbens shell, a brain region considered important for the reinforcing effects of abused drugs. -
Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?
REVIEW published: 21 November 2019 doi: 10.3389/fpsyt.2019.00835 Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type? Alexei M. Bygrave 1, Kasyoka Kilonzo 2, Dimitri M. Kullmann 3, David M. Bannerman 4 and Dennis Kätzel 2* 1 Department of Neuroscience, Johns Hopkins University, Baltimore, MD, United States, 2 Institute of Applied Physiology, Ulm University, Ulm, Germany, 3 UCL Queen Square Institute of Neurology, University College London, London, United Kingdom, 4 Department of Experimental Psychology, University of Oxford, Oxford, United Kingdom Hypofunction of N-methyl-D-aspartate glutamate receptors (NMDARs), whether caused by endogenous factors like auto-antibodies or mutations, or by pharmacological or genetic manipulations, produces a wide variety of deficits which overlap with—but do not precisely match—the symptom spectrum of schizophrenia. In order to understand how NMDAR hypofunction leads to different components of the syndrome, it is necessary to take into account which neuronal subtypes are particularly affected by it in terms of detrimental Edited by: functional alterations. We provide a comprehensive overview detailing findings in rodent Bernat Kocsis, Harvard Medical School, models with cell type–specific knockout of NMDARs. Regarding inhibitory cortical cells, United States an emerging model suggests that NMDAR hypofunction in parvalbumin (PV) positive Reviewed by: interneurons is a potential risk factor for this disease. PV interneurons display a selective Margarita Behrens, Salk Institute for Biological Studies, vulnerability resulting from a combination of genetic, cellular, and environmental factors United States that produce pathological multi-level positive feedback loops. Central to this are two Vasileios Kafetzopoulos, antioxidant mechanisms—NMDAR activity and perineuronal nets—which are themselves Harvard Medical School, United States impaired by oxidative stress, amplifying disinhibition. -
RTI-4793-14, a New Ligand with High Affinity and Selectivity For
SYNAPSE 16:59-65 (1994) RTI-4793-14, a New Ligand With High Affinity and Selectivity for the ( +)-MK801-Insensitive [3H]1 -[ 1 -( 2- thienyl)cyclohexyl]piperidine Binding Site (PCP Site 2) of Guinea Pig Brain CARL B. GOODMAN, D. NIGEL THOMAS, AGU PERT, BETSEY EMILIEN, JEAN L. CADET, F. IVY CARROLL, BRUCE E. BLOUGH, S. WAYNE MASCARELLA, MICHAEL A. ROGAWSKI, SWAMINATHAN SUBRAMANIAM, AM) RICHARD B. ROTHMAN Clinical Psychopharmacology Section, NIDMNIH Addiction Research Center, Baltimore, Maryland 21224 (C.B.G., B.E., J.L.C., R.B.R.); Biological Psychiatry Branch, NZMH (D.N.T., A.P.) and Neuronal Excitability Section, Epilepsy Research Branch, NINDS (M.A.R., S.S.), NIH, Bethesda, Maryland 20892; and Chemistry and Life Sciences, Organic and Medicinal Chemistry, Research Triangle Institute, Research Triangle Park, North Carolina 27709-2194 (F.I.C., B.E.B., S.W.M.) KEY WORDS Phencyclidine receptor, RTI-4793-14, PCP, Biogenic amine reuptake carrier, ( + )-MK801, Guinea pig brain ABSTRACT L3HlTCP, an analog of the dissociative anesthetic phencyclidine (PCP), binds with high affinity to two sites in guinea pig brain membranes, one that is MK-801 sensitive and one that is not. The MK-801-sensitive site (PCP site 1) is associated with NMDA receptors, whereas the MK-801-insensitive site (PCP site 2) may be associated with biogenic amine transporters (BAT).Although several “BAT ligands” are known that bind selectively to PCP site 2 and not to PCP site 1 (such as indatraline), these corn- pounds have low affinity for site 2 (K, values > 1 pM). Here we demonstrate that the novel pyrrole RTI-4793-14 is a selective, high affinity ligand for PCP site 2. -
From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia J
REVIEW The Neuropsychopharmacology of Phencyclidine: From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia J. David Jentsch, Ph.D., and Robert H. Roth, Ph.D. Administration of noncompetitive NMDA/glutamate effects of these drugs are discussed, especially with regard to receptor antagonists, such as phencyclidine (PCP) and differing profiles following single-dose and long-term ketamine, to humans induces a broad range of exposure. The neurochemical effects of NMDA receptor schizophrenic-like symptomatology, findings that have antagonist administration are argued to support a contributed to a hypoglutamatergic hypothesis of neurobiological hypothesis of schizophrenia, which includes schizophrenia. Moreover, a history of experimental pathophysiology within several neurotransmitter systems, investigations of the effects of these drugs in animals manifested in behavioral pathology. Future directions for suggests that NMDA receptor antagonists may model some the application of NMDA receptor antagonist models of behavioral symptoms of schizophrenia in nonhuman schizophrenia to preclinical and pathophysiological research subjects. In this review, the usefulness of PCP are offered. [Neuropsychopharmacology 20:201–225, administration as a potential animal model of schizophrenia 1999] © 1999 American College of is considered. To support the contention that NMDA Neuropsychopharmacology. Published by Elsevier receptor antagonist administration represents a viable Science Inc. model of schizophrenia, the behavioral and neurobiological KEY WORDS: Ketamine; Phencyclidine; Psychotomimetic; widely from the administration of purportedly psychot- Memory; Catecholamine; Schizophrenia; Prefrontal cortex; omimetic drugs (Snyder 1988; Javitt and Zukin 1991; Cognition; Dopamine; Glutamate Jentsch et al. 1998a), to perinatal insults (Lipska et al. Biological psychiatric research has seen the develop- 1993; El-Khodor and Boksa 1997; Moore and Grace ment of many putative animal models of schizophrenia. -
Chapter 1—— IBOGAINE: a REVIEW
——Chapter 1—— IBOGAINE: A REVIEW Kenneth R. Alper Departments of Psychiatry and Neurology New York University School of Medicine New York, NY 10016 I. Introduction, Chemical Properties, and Historical Time Line .................................... A. Introduction............................................................................................................ B. Chemical Structure and Properties ........................................................................ C. Historical Time Line.............................................................................................. II. Mechanisms of Action ................................................................................................. A. Neurotransmitter Activities.................................................................................... B. Discrimination Studies........................................................................................... C. Effects on Neuropeptides....................................................................................... D. Possible Effects on Neuroadaptations Related to Drug Sensitization or Tolerance ........................................................................................................... III. Evidence of Efficacy in Animal Models....................................................................... A. Drug Self-Administration ...................................................................................... B. Acute Opioid Withdrawal..................................................................................... -
Self-Administration of Abused Substances: Methods for Study
Self-Administration of Abused Substances: Methods for Study U.S. DEPARTMENT OF HEALTH, EDUCATION AND WELFARE Public Health Service Alcohol, Drug Abuse, and Mental Health Administration Self-Administration of Abused Substances: Methods for Study Editor: Norman A. Krasnegor, Ph.D. NIDA Research Monograph 20 July 1978 DEPARTMENT OF HEALTH. EDUCATION, AND WELFARE Public Health Service Alcohol, Drug Abuse, and Mental Health Administration National Institute on Drug Abuse Division of Research 5600 Fishers Lane Rockville, Maryland 20857 For sale by the Superintendent of Documents U.S. Government Printing Office, Washington, D.C. 20402 Stock No. 017-024-00794-3 The NIDA Research Monograph series is prepared by the Division of Research of the National Institute on Drug Abuse. Its primary objective is to provide critical re- views of research problem areas and techniques, the content of state-of-the-art conferences, integrative research reviews and significant original research. Its dual publication emphasis is rapid and targeted dissemination to the scientific and professional community. Editorial Advisory Board Avram Goldstein, M.D. Addiction Research Foundation Polo Alto, California Jerome Jaffe, M.D. College of Physicians and Surgeons Columbia University New York Reese T. Jones, M.D. Langley Porter Neuropsychiatric Institute University of California San Francisco, California William McGlothlin, Ph.D. Department of Psychology. UCLA Los Angeles, California Jack Mendelson, M.D. Alcohol and Drug Abuse Research Center Harvard Medical School McLean Hospital Belmont, Massachusetts Helen Nowlis, Ph.D. Office of Drug Education, DHEW Washington, D C Lee Robins, Ph.D. Washington University School of Medicine St Louis, Missouri NIDA Research Monograph series William Pollin, M.D. -
Problems of Drug Dependence 1980 Proceedings of the 42Nd Annual Scientific Meeting the Committee on Problems of Drug Dependence
National Institute on Drug Abuse MONOGRAPH SERIES Problems of Drug Dependence 1980 Proceedings of the 42nd Annual Scientific Meeting The Committee on Problems of Drug Dependence, Inc. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES • Public Health Service • Alcohol, Drug Abuse, and Mental Health Administration Problems of Drug Dependence, 1980 Proceedings of the 42nd Annual Scientific Meeting, The Committee on Problems of Drug Dependence, Inc. Editor: Louis S. Harris, Ph.D. NIDA Research Monograph 34 February 1981 DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Alcohol, Drug Abuse, and Mental Health Administration National Institute on Drug Abuse Division of Research 5600 Fishers Lane Rockville, Maryland 20857 For sale by the Superintendent of Documents, U.S. Government Printing Office Washington, D.C. 20402 The NIDA Research Monograph series is prepared by the Division of Research of the National Institute on Drug Abuse. Its primary objective is to provide critical reviews of research problem areas and techniques, the content of state-of-the-art conferences, integrative research reviews and significant original research. Its dual publication emphasis is rapid and targeted dissemination to the scientific and professional community. Editorial Advisory Board Avram Goldstein, M.D. Addiction Research Foundation Palo Alto, California Jerome Jaffe, M.D. College of Physicians and Surgeons Columbia University, New York Reese T. Jones, M.D. Langley Porter Neuropsychiatric Institute University of California San Francisco, California William McGlothlin, Ph.D. Deportment of Psychology, UCLA Los Angeles, California Jack Mendelson, M.D. Alcohol and Drug Abuse Research Center Harvard Medical School McLean Hospital Belmont, Massachusetts Helen Nowlis, Ph.D. Office of Drug Education, DHHS Washington, D.C Lee Robins, Ph.D. -
DEMAND REDUCTION a Glossary of Terms
UNITED NATIONS PUBLICATION Sales No. E.00.XI.9 ISBN: 92-1-148129-5 ACKNOWLEDGEMENTS This document was prepared by the: United Nations International Drug Control Programme (UNDCP), Vienna, Austria, in consultation with the Commonwealth of Health and Aged Care, Australia, and the informal international reference group. ii Contents Page Foreword . xi Demand reduction: A glossary of terms . 1 Abstinence . 1 Abuse . 1 Abuse liability . 2 Action research . 2 Addiction, addict . 2 Administration (method of) . 3 Adverse drug reaction . 4 Advice services . 4 Advocacy . 4 Agonist . 4 AIDS . 5 Al-Anon . 5 Alcohol . 5 Alcoholics Anonymous (AA) . 6 Alternatives to drug use . 6 Amfetamine . 6 Amotivational syndrome . 6 Amphetamine . 6 Amyl nitrate . 8 Analgesic . 8 iii Page Antagonist . 8 Anti-anxiety drug . 8 Antidepressant . 8 Backloading . 9 Bad trip . 9 Barbiturate . 9 Benzodiazepine . 10 Blood-borne virus . 10 Brief intervention . 11 Buprenorphine . 11 Caffeine . 12 Cannabis . 12 Chasing . 13 Cocaine . 13 Coca leaves . 14 Coca paste . 14 Cold turkey . 14 Community empowerment . 15 Co-morbidity . 15 Comprehensive Multidisciplinary Outline of Future Activities in Drug Abuse Control (CMO) . 15 Controlled substance . 15 Counselling and psychotherapy . 16 Court diversion . 16 Crash . 16 Cross-dependence . 17 Cross-tolerance . 17 Custody diversion . 17 Dance drug . 18 Decriminalization or depenalization . 18 Demand . 18 iv Page Demand reduction . 19 Dependence, dependence syndrome . 19 Dependence liability . 20 Depressant . 20 Designer drug . 20 Detoxification . 20 Diacetylmorphine/Diamorphine . 21 Diuretic . 21 Drug . 21 Drug abuse . 22 Drug abuse-related harm . 22 Drug abuse-related problem . 22 Drug policy . 23 Drug seeking . 23 Drug substitution . 23 Drug testing . 24 Drug use . -
Gαq-ASSOCIATED SIGNALING PROMOTES NEUROADAPTATION to ETHANOL and WITHDRAWAL-ASSOCIATED HIPPOCAMPAL DAMAGE
University of Kentucky UKnowledge Theses and Dissertations--Psychology Psychology 2015 Gαq-ASSOCIATED SIGNALING PROMOTES NEUROADAPTATION TO ETHANOL AND WITHDRAWAL-ASSOCIATED HIPPOCAMPAL DAMAGE Anna R. Reynolds Univerity of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Reynolds, Anna R., "Gαq-ASSOCIATED SIGNALING PROMOTES NEUROADAPTATION TO ETHANOL AND WITHDRAWAL-ASSOCIATED HIPPOCAMPAL DAMAGE" (2015). Theses and Dissertations--Psychology. 74. https://uknowledge.uky.edu/psychology_etds/74 This Doctoral Dissertation is brought to you for free and open access by the Psychology at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Psychology by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known. I agree that the document mentioned above may be made available immediately for worldwide access unless an embargo applies. -
Hallucinogens & Dissociative Drugs
® DRUG FACT SHEET Hallucinogens & Dissociative Drugs Some effects of PCP including depression and memory loss may last six months to a year following prolonged daily use. Class of drug: Hallucinogens (most common form is LSD) Dissociative drugs (most commonly form is PCP) Main active ingredient: Hallucinogens: Lysergic acid diethylamide, mescaline, psilocybin, ibogaine Dissociative: Phencyclidine What it looks like: LSD: Clear, odorless liquid, brightly colored tablets, impregnated blotter paper, thin squares of gelatin PCP: liquid, capsules, white crystalline powder, gum There are hundreds of synthetic hallu - Street names: Lysergic acid diethylamide: LSD, Acid, Blotter, cinogens on the market today including Phencyclidine: PCP, Angel Dust, Loveboat, Wack 25I-NBOMe (N-Bomb) and 2C-I (Smiles) which have been attributed to How it is used: Both hallucinogens and dissociative drugs can be multiple deaths and significant injuries. swallowed, injected or smoked. LSD liquid and gelatin They are generally found as powders, liq - forms can be put in the eyes. PCP is often sprinkled uids, soaked into blotter paper or laced on or sprayed on cigarettes, parsley and marijuana. something edible. Both drugs are classi - fied as Schedule I substances, making Duration of high: Hallucinogens: effects begin within 30 to 90 minutes possession, distribution and manufacture and last from six to twelve hours illegal. PCP: effects begin within minutes and last for hours Withdrawal symptoms: Depression, memory loss U.S. information Effects: Physical (both) —increased heart rate and blood pressure, elevated body temperature, loss of In 2014, nearly 1.3 million appetite, loss of muscle coordination, slurred speech Americans aged 12 and older Hallucinogens reported using LSD in the past Mental —hallucinations; intensified senses; distortion year and 90,000 reported using of time, reality and environment; confusion; mood PCP in the past year.