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Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure

Binge drinking damages the brain, and although a significant amount of recovery occurs with abstinence, there is a need for effective strategies to maximize neurorestoration. In contrast to binge drinking, exercise promotes brain health, so the present study assessed whether it could counteract etha...

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Autores principales: Maynard, Mark E., Leasure, J. Leigh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786922/
https://www.ncbi.nlm.nih.gov/pubmed/24098797
http://dx.doi.org/10.1371/journal.pone.0076644
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author Maynard, Mark E.
Leasure, J. Leigh
author_facet Maynard, Mark E.
Leasure, J. Leigh
author_sort Maynard, Mark E.
collection PubMed
description Binge drinking damages the brain, and although a significant amount of recovery occurs with abstinence, there is a need for effective strategies to maximize neurorestoration. In contrast to binge drinking, exercise promotes brain health, so the present study assessed whether it could counteract ethanol-induced damage by augmenting natural self-repair processes following one or more binge exposures. Adult female rats were exposed to 0 (control), 1 or 2 binges, using an established 4-day model of binge-induced neurodegeneration. Half of the animals in each group remained sedentary, or had running wheel access beginning 7 days after the final binge, and were sacrificed 28 days later. To assess binge-induced hippocampal damage and exercise restoration, we quantified volume of the dentate gyrus and number of granule neurons. We found that a single binge exposure significantly decreased the volume of the dentate gyrus and number of granule neurons. A second binge did not exacerbate the damage. Exercise completely restored baseline volume and granule neuron numbers. To investigate a potential mechanism of this restoration, we administered IdU (a thymidine analog) in order to label cells generated after the first binge. Previous studies have shown that neurogenesis in the dentate gyrus is decreased by binge alcohol exposure, and that the hippocampus responds to this insult by increasing cell genesis during abstinence. We found increased IdU labeling in binge-exposed animals, and a further increase in binged animals that exercised. Our results indicate that exercise reverses long-lasting hippocampal damage by augmenting natural self-repair processes.
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spelling pubmed-37869222013-10-04 Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure Maynard, Mark E. Leasure, J. Leigh PLoS One Research Article Binge drinking damages the brain, and although a significant amount of recovery occurs with abstinence, there is a need for effective strategies to maximize neurorestoration. In contrast to binge drinking, exercise promotes brain health, so the present study assessed whether it could counteract ethanol-induced damage by augmenting natural self-repair processes following one or more binge exposures. Adult female rats were exposed to 0 (control), 1 or 2 binges, using an established 4-day model of binge-induced neurodegeneration. Half of the animals in each group remained sedentary, or had running wheel access beginning 7 days after the final binge, and were sacrificed 28 days later. To assess binge-induced hippocampal damage and exercise restoration, we quantified volume of the dentate gyrus and number of granule neurons. We found that a single binge exposure significantly decreased the volume of the dentate gyrus and number of granule neurons. A second binge did not exacerbate the damage. Exercise completely restored baseline volume and granule neuron numbers. To investigate a potential mechanism of this restoration, we administered IdU (a thymidine analog) in order to label cells generated after the first binge. Previous studies have shown that neurogenesis in the dentate gyrus is decreased by binge alcohol exposure, and that the hippocampus responds to this insult by increasing cell genesis during abstinence. We found increased IdU labeling in binge-exposed animals, and a further increase in binged animals that exercised. Our results indicate that exercise reverses long-lasting hippocampal damage by augmenting natural self-repair processes. Public Library of Science 2013-09-30 /pmc/articles/PMC3786922/ /pubmed/24098797 http://dx.doi.org/10.1371/journal.pone.0076644 Text en © 2013 Maynard and Leasure http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Maynard, Mark E.
Leasure, J. Leigh
Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure
title Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure
title_full Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure
title_fullStr Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure
title_full_unstemmed Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure
title_short Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure
title_sort exercise enhances hippocampal recovery following binge ethanol exposure
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786922/
https://www.ncbi.nlm.nih.gov/pubmed/24098797
http://dx.doi.org/10.1371/journal.pone.0076644
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