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Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects
BACKGROUND: Cycles of alcohol and stress are hypothesized to contribute to alcohol use disorders. How this occurs is poorly understood, although both alcohol and stress activate the neuroimmune system—the immune molecules and cells that interact with the nervous system. The effects of alcohol and st...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5725687/ https://www.ncbi.nlm.nih.gov/pubmed/28941277 http://dx.doi.org/10.1111/acer.13511 |
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author | Walter, Thomas Jordan Vetreno, Ryan P. Crews, Fulton T. |
author_facet | Walter, Thomas Jordan Vetreno, Ryan P. Crews, Fulton T. |
author_sort | Walter, Thomas Jordan |
collection | PubMed |
description | BACKGROUND: Cycles of alcohol and stress are hypothesized to contribute to alcohol use disorders. How this occurs is poorly understood, although both alcohol and stress activate the neuroimmune system—the immune molecules and cells that interact with the nervous system. The effects of alcohol and stress on the neuroimmune system are mediated in part by peripheral signaling molecules. Alcohol and stress both enhance immunomodulatory molecules such as corticosterone and endotoxin to impact neuroimmune cells, such as microglia, and may subsequently impact neurons. In this study, we therefore examined the effects of acute and chronic ethanol (EtOH) on the corticosterone, endotoxin, and microglial and neuronal response to acute stress. METHODS: Male Wistar rats were treated intragastrically with acute EtOH and acutely stressed with restraint/water immersion. Another group of rats was treated intragastrically with chronic intermittent EtOH and acutely stressed following prolonged abstinence. Plasma corticosterone and endotoxin were measured, and immunohistochemical stains for the microglial marker CD11b and neuronal activation marker c‐Fos were performed. RESULTS: Acute EtOH and acute stress interacted to increase plasma endotoxin and microglial CD11b, but not plasma corticosterone or neuronal c‐Fos. Chronic EtOH caused a lasting sensitization of stress‐induced plasma endotoxin, but not plasma corticosterone. Chronic EtOH also caused a lasting sensitization of stress‐induced microglial CD11b, but not neuronal c‐Fos. CONCLUSIONS: These results find acute EtOH combined with acute stress enhanced plasma endotoxin, as well as microglial CD11b in many brain regions. Chronic EtOH followed by acute stress also increased plasma endotoxin and microglial CD11b, suggesting a lasting sensitization to acute stress. Overall, these data suggest alcohol and stress interact to increase plasma endotoxin, resulting in enhanced microglial activation that could contribute to disease progression. |
format | Online Article Text |
id | pubmed-5725687 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57256872017-12-12 Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects Walter, Thomas Jordan Vetreno, Ryan P. Crews, Fulton T. Alcohol Clin Exp Res Cell and Molecular Biology BACKGROUND: Cycles of alcohol and stress are hypothesized to contribute to alcohol use disorders. How this occurs is poorly understood, although both alcohol and stress activate the neuroimmune system—the immune molecules and cells that interact with the nervous system. The effects of alcohol and stress on the neuroimmune system are mediated in part by peripheral signaling molecules. Alcohol and stress both enhance immunomodulatory molecules such as corticosterone and endotoxin to impact neuroimmune cells, such as microglia, and may subsequently impact neurons. In this study, we therefore examined the effects of acute and chronic ethanol (EtOH) on the corticosterone, endotoxin, and microglial and neuronal response to acute stress. METHODS: Male Wistar rats were treated intragastrically with acute EtOH and acutely stressed with restraint/water immersion. Another group of rats was treated intragastrically with chronic intermittent EtOH and acutely stressed following prolonged abstinence. Plasma corticosterone and endotoxin were measured, and immunohistochemical stains for the microglial marker CD11b and neuronal activation marker c‐Fos were performed. RESULTS: Acute EtOH and acute stress interacted to increase plasma endotoxin and microglial CD11b, but not plasma corticosterone or neuronal c‐Fos. Chronic EtOH caused a lasting sensitization of stress‐induced plasma endotoxin, but not plasma corticosterone. Chronic EtOH also caused a lasting sensitization of stress‐induced microglial CD11b, but not neuronal c‐Fos. CONCLUSIONS: These results find acute EtOH combined with acute stress enhanced plasma endotoxin, as well as microglial CD11b in many brain regions. Chronic EtOH followed by acute stress also increased plasma endotoxin and microglial CD11b, suggesting a lasting sensitization to acute stress. Overall, these data suggest alcohol and stress interact to increase plasma endotoxin, resulting in enhanced microglial activation that could contribute to disease progression. John Wiley and Sons Inc. 2017-11-08 2017-12 /pmc/articles/PMC5725687/ /pubmed/28941277 http://dx.doi.org/10.1111/acer.13511 Text en Copyright © 2017 The Authors Alcoholism: Clinical & Experimental Research published by Wiley Periodicals, Inc. on behalf of Research Society on Alcoholism This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial (http://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Cell and Molecular Biology Walter, Thomas Jordan Vetreno, Ryan P. Crews, Fulton T. Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects |
title | Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects |
title_full | Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects |
title_fullStr | Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects |
title_full_unstemmed | Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects |
title_short | Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects |
title_sort | alcohol and stress activation of microglia and neurons: brain regional effects |
topic | Cell and Molecular Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5725687/ https://www.ncbi.nlm.nih.gov/pubmed/28941277 http://dx.doi.org/10.1111/acer.13511 |
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