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Methamphetamine neurotoxicity, microglia, and neuroinflammation
Methamphetamine (METH) is an illicit psychostimulant that is subject to abuse worldwide. While the modulatory effects of METH on dopamine neurotransmission and its neurotoxicity in the central nervous system are well studied, METH’s effects on modulating microglial neuroimmune functions and on elici...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292109/ https://www.ncbi.nlm.nih.gov/pubmed/30541633 http://dx.doi.org/10.1186/s12974-018-1385-0 |
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author | Shaerzadeh, Fatemeh Streit, Wolfgang J. Heysieattalab, Soomaayeh Khoshbouei, Habibeh |
author_facet | Shaerzadeh, Fatemeh Streit, Wolfgang J. Heysieattalab, Soomaayeh Khoshbouei, Habibeh |
author_sort | Shaerzadeh, Fatemeh |
collection | PubMed |
description | Methamphetamine (METH) is an illicit psychostimulant that is subject to abuse worldwide. While the modulatory effects of METH on dopamine neurotransmission and its neurotoxicity in the central nervous system are well studied, METH’s effects on modulating microglial neuroimmune functions and on eliciting neuroinflammation to affect dopaminergic neurotoxicity has attracted considerable attention in recent years. The current review illuminates METH-induced neurotoxicity from a neuropathological perspective by summarizing studies reporting microglial activation after METH administration in rodents. Assessing microglial reactivity in terms of the cells’ morphology and immunophenotype offers an opportunity for comprehensive and objective assessment of the severity and nature of METH-induced neuronal perturbations in the CNS and can thus contribute to a better understanding of the nature of METH toxicity. We reach the conclusion here that the intensity of microglial activation reported in the majority of animal models after METH administration is quite modest, indicating that the extent of dopaminergic neuron damage directly caused by this neurotoxicant is relatively minor. Our conclusion stands in contrast to claims of excessive and detrimental neuroinflammation believed to contribute and exacerbate METH neurotoxicity. Thus, our analysis of published studies does not support the idea that suppression of microglial activity with anti-inflammatory agents could yield beneficial effects in terms of treating addiction disorders. |
format | Online Article Text |
id | pubmed-6292109 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-62921092018-12-17 Methamphetamine neurotoxicity, microglia, and neuroinflammation Shaerzadeh, Fatemeh Streit, Wolfgang J. Heysieattalab, Soomaayeh Khoshbouei, Habibeh J Neuroinflammation Review Methamphetamine (METH) is an illicit psychostimulant that is subject to abuse worldwide. While the modulatory effects of METH on dopamine neurotransmission and its neurotoxicity in the central nervous system are well studied, METH’s effects on modulating microglial neuroimmune functions and on eliciting neuroinflammation to affect dopaminergic neurotoxicity has attracted considerable attention in recent years. The current review illuminates METH-induced neurotoxicity from a neuropathological perspective by summarizing studies reporting microglial activation after METH administration in rodents. Assessing microglial reactivity in terms of the cells’ morphology and immunophenotype offers an opportunity for comprehensive and objective assessment of the severity and nature of METH-induced neuronal perturbations in the CNS and can thus contribute to a better understanding of the nature of METH toxicity. We reach the conclusion here that the intensity of microglial activation reported in the majority of animal models after METH administration is quite modest, indicating that the extent of dopaminergic neuron damage directly caused by this neurotoxicant is relatively minor. Our conclusion stands in contrast to claims of excessive and detrimental neuroinflammation believed to contribute and exacerbate METH neurotoxicity. Thus, our analysis of published studies does not support the idea that suppression of microglial activity with anti-inflammatory agents could yield beneficial effects in terms of treating addiction disorders. BioMed Central 2018-12-12 /pmc/articles/PMC6292109/ /pubmed/30541633 http://dx.doi.org/10.1186/s12974-018-1385-0 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Shaerzadeh, Fatemeh Streit, Wolfgang J. Heysieattalab, Soomaayeh Khoshbouei, Habibeh Methamphetamine neurotoxicity, microglia, and neuroinflammation |
title | Methamphetamine neurotoxicity, microglia, and neuroinflammation |
title_full | Methamphetamine neurotoxicity, microglia, and neuroinflammation |
title_fullStr | Methamphetamine neurotoxicity, microglia, and neuroinflammation |
title_full_unstemmed | Methamphetamine neurotoxicity, microglia, and neuroinflammation |
title_short | Methamphetamine neurotoxicity, microglia, and neuroinflammation |
title_sort | methamphetamine neurotoxicity, microglia, and neuroinflammation |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292109/ https://www.ncbi.nlm.nih.gov/pubmed/30541633 http://dx.doi.org/10.1186/s12974-018-1385-0 |
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