RGD Reference Report - Upregulated vimentin suggests new areas of neurodegeneration in a model of an alcohol use disorder. - Rat Genome Database

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Upregulated vimentin suggests new areas of neurodegeneration in a model of an alcohol use disorder.

Authors: Kelso, ML  Liput, DJ  Eaves, DW  Nixon, K 
Citation: Kelso ML, etal., Neuroscience. 2011 Dec 1;197:381-93. Epub 2011 Sep 16.
RGD ID: 6480622
Pubmed: PMID:21958862   (View Abstract at PubMed)
PMCID: PMC3298440   (View Article at PubMed Central)
DOI: DOI:10.1016/j.neuroscience.2011.09.019   (Journal Full-text)

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.



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Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
VIMHumanGliosis  ISOVim (Rattus norvegicus)associated with alcohol-induced disorders, nervous system;protein:increased expression:astrocyteRGD 
VimRatGliosis  IEP associated with alcohol-induced disorders, nervous system;protein:increased expression:astrocyteRGD 
VimMouseGliosis  ISOVim (Rattus norvegicus)associated with alcohol-induced disorders, nervous system;protein:increased expression:astrocyteRGD 

Objects Annotated

Genes (Rattus norvegicus)
Vim  (vimentin)

Genes (Mus musculus)
Vim  (vimentin)

Genes (Homo sapiens)
VIM  (vimentin)


Additional Information