Document Detail


Upregulated vimentin suggests new areas of neurodegeneration in a model of an alcohol use disorder.
MedLine Citation:
PMID:  21958862     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Excessive alcohol intake, characteristic of an alcohol use disorder (AUD), results in neurodegeneration as well as cognitive deficits that may recover in abstinence. Neurodegeneration in psychiatric disorders such as AUDs is due to various effects on tissue integrity. Several groups report that alcohol-induced neurodegeneration and recovery include a role for adult neurogenesis. Therefore, the initial purpose of this study was to investigate the effect of alcohol on the temporal profile of neural progenitor cells using the radial glia marker, vimentin, in a model of an AUD. However, striking vimentin expression throughout corticolimbic regions led, instead, to the discovery of a significant gliosis response in this model. Adult male rats were subjected to a 4-day binge model of an AUD and brains harvested for immunohistochemistry at 0, 2, 4, 7, 14, and 28 days following the last dose of ethanol. A prominent increase in vimentin immunoreactivity was apparent at 4 and 7 days post binge that returned to control levels by 14 days in the corticolimbic regions examined. Vimentin-positive cells co-labeled with glial fibrillary acidic protein (GFAP), which suggested that cells were reactive astrocytes. A second experiment supported that increased vimentin was not primarily due to alcohol withdrawal seizures and is more likely due to alcohol-induced cell death. As this gliosis was remarkably distinct in regions where cell death had not previously been reported in this model, adjacent tissue sections were processed for FluoroJade B staining for cell death. FluoroJade B-positive cells were evident immediately following the last ethanol dose as expected, but were significantly elevated in the hippocampal dentate gyrus and CA3 regions and corticolimbic regions from 2 to 7 days post binge. Intriguingly, vimentin labeling of astrogliosis is more widespread than FluoroJade B labeling of cell death, which suggests that 4-day binge ethanol consumption is more damaging than originally realized.
Authors:
M L Kelso; D J Liput; D W Eaves; K Nixon
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-09-16
Journal Detail:
Title:  Neuroscience     Volume:  197     ISSN:  1873-7544     ISO Abbreviation:  Neuroscience     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-11-07     Completed Date:  2012-02-27     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  381-93     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Alcoholism / physiopathology*
Animals
Brain / metabolism,  physiopathology*
Disease Models, Animal
Gliosis / chemically induced*,  metabolism,  physiopathology
Immunohistochemistry
Male
Nerve Degeneration / chemically induced*,  metabolism,  physiopathology
Neural Stem Cells / metabolism,  pathology
Rats
Rats, Sprague-Dawley
Up-Regulation
Vimentin / biosynthesis*
Grant Support
ID/Acronym/Agency:
F31 AA019853/AA/NIAAA NIH HHS; P60 AA011605/AA/NIAAA NIH HHS; P60 AA011605-08/AA/NIAAA NIH HHS; P60AA011605/AA/NIAAA NIH HHS; R01 AA016959/AA/NIAAA NIH HHS; R01 AA016959-01/AA/NIAAA NIH HHS; R01AA016959/AA/NIAAA NIH HHS; T32 DA016176/DA/NIDA NIH HHS; T32 DA016176-06/DA/NIDA NIH HHS; T32DA016176/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/Vimentin
Comments/Corrections

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