The neurobiology of methamphetamine induced psychosis

Chronic methamphetamine abuse commonly leads to psychosis, with positive and cognitive symptoms that are similar to those of schizophrenia. Methamphetamine induced psychosis (MAP) can persist and diagnoses of MAP often change to a diagnosis of schizophrenia over time. Studies in schizophrenia have f...

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Bibliographic Details
Published inFrontiers in human neuroscience Vol. 8; p. 537
Main Authors Hsieh, Jennifer H, Stein, Dan J, Howells, Fleur M
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 22.07.2014
Frontiers Media S.A
Subjects
Amphetamines
Cocaine
Cognitive ability
Cortex
Dopamine
Dopamine receptors
Drug abuse
Drug dosages
GABA
Glutamic acid receptors (ionotropic)
Interneurons
Memory
Mental disorders
Methamphetamine
Monkeys & apes
N-Methyl-D-aspartic acid receptors
Nervous system
neural circuits
Neuroscience
Neurosciences
Neurotoxicity
Psychiatry
Psychosis
Receptor mechanisms
Schizophrenia
sensitization
Thailand
cortex
GABA
neurotoxicity
schizophrenia
sensitization
neural circuitry
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Summary:Chronic methamphetamine abuse commonly leads to psychosis, with positive and cognitive symptoms that are similar to those of schizophrenia. Methamphetamine induced psychosis (MAP) can persist and diagnoses of MAP often change to a diagnosis of schizophrenia over time. Studies in schizophrenia have found much evidence of cortical GABAergic dysfunction. Methamphetamine psychosis is a well studied model for schizophrenia, however there is little research on the effects of methamphetamine on cortical GABAergic function in the model, and the neurobiology of MAP is unknown. This paper reviews the effects of methamphetamine on dopaminergic pathways, with focus on its ability to increase glutamate release in the cortex. Excess cortical glutamate would likely damage GABAergic interneurons, and evidence of this disturbance as a result of methamphetamine treatment will be discussed. We propose that cortical GABAergic interneurons are particularly vulnerable to glutamate overflow as a result of subcellular location of NMDA receptors on interneurons in the cortex. Damage to cortical GABAergic function would lead to dysregulation of cortical signals, resulting in psychosis, and further support MAP as a model for schizophrenia.
Bibliography:Edited by: Anneke E. Goudriaan, University of Amsterdam and Arkin Mental Health, Netherlands
Reviewed by: Gregg Stanwood, Vanderbilt University, USA; Ali Mazaheri, University of Amsterdam, USA; Nitya Jayaram-Lindstrom, Karolinska Institutet, Sweden
This article was submitted to the journal Frontiers in Human Neuroscience.
ISSN:1662-5161
1662-5161
DOI:10.3389/fnhum.2014.00537