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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2014-07-01
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doaj-a99e8d28615b4863bfabc7d6993b16aa2020-11-25T03:23:44ZengFrontiers Media S.A.Frontiers in Human Neuroscience1662-51612014-07-01810.3389/fnhum.2014.0053780393The Neurobiology of Methamphetamine Induced PsychosisJennifer Hsin-Wen Hsieh0Dan J Stein1Fleur Margaret Howells2University of Cape TownUniversity of Cape TownUniversity of Cape TownChronic 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 methamphetamine induced psychosis as a model for schizophrenia.http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.00537/fullSchizophreniaGABACortexNeurotoxicityneural circuitssensitization |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jennifer Hsin-Wen Hsieh Dan J Stein Fleur Margaret Howells |
spellingShingle |
Jennifer Hsin-Wen Hsieh Dan J Stein Fleur Margaret Howells The Neurobiology of Methamphetamine Induced Psychosis Frontiers in Human Neuroscience Schizophrenia GABA Cortex Neurotoxicity neural circuits sensitization |
author_facet |
Jennifer Hsin-Wen Hsieh Dan J Stein Fleur Margaret Howells |
author_sort |
Jennifer Hsin-Wen Hsieh |
title |
The Neurobiology of Methamphetamine Induced Psychosis |
title_short |
The Neurobiology of Methamphetamine Induced Psychosis |
title_full |
The Neurobiology of Methamphetamine Induced Psychosis |
title_fullStr |
The Neurobiology of Methamphetamine Induced Psychosis |
title_full_unstemmed |
The Neurobiology of Methamphetamine Induced Psychosis |
title_sort |
neurobiology of methamphetamine induced psychosis |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Human Neuroscience |
issn |
1662-5161 |
publishDate |
2014-07-01 |
description |
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 methamphetamine induced psychosis as a model for schizophrenia. |
topic |
Schizophrenia GABA Cortex Neurotoxicity neural circuits sensitization |
url |
http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.00537/full |
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