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Published in: Translational Stroke Research 3/2011

01-09-2011 | Original Article

Expression of Histone Deacetylases in Cellular Compartments of the Mouse Brain and the Effects of Ischemia

Authors: Selva Baltan, Amelia Bachleda, Richard S. Morrison, Sean P. Murphy

Published in: Translational Stroke Research | Issue 3/2011

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Abstract

Drugs that inhibit specific histone deacetylase (HDAC) activities have enormous potential in preventing the consequences of acute injury to the nervous system and in allaying neurodegeneration. However, very little is known about the expression pattern of the HDACs in the central nervous system (CNS). Identifying the cell types that express HDACs in the CNS is important for determining therapeutic targets for HDAC inhibitors and evaluating potential side effects. We characterized the cellular expression of HDACs 1–3, and HDACs 4 and 6, in the adult mouse brain in the cingulate cortex, parietal cortex, dentate gyrus, and CA1 regions of the hippocampus and subcortical white matter. Expression of class I HDACs showed a cell- and region-specific pattern. Transient focal ischemia induced by temporary middle cerebral artery occlusion, or global ischemia induced by in vitro oxygen–glucose deprivation, altered the extent of HDAC expression in a region- and cell-specific manner. The pan-HDAC inhibitor, SAHA, reduced ischemia-induced alterations in HDACs. The results suggest that in addition to promoting epigenetic changes in transcriptional activity in the nucleus of neurons and glia, HDACs may also have non-transcriptional actions in axons and the distant processes of glial cells and may significantly modulate the response to injury in a cell- and region-specific manner.
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Metadata
Title
Expression of Histone Deacetylases in Cellular Compartments of the Mouse Brain and the Effects of Ischemia
Authors
Selva Baltan
Amelia Bachleda
Richard S. Morrison
Sean P. Murphy
Publication date
01-09-2011
Publisher
Springer-Verlag
Published in
Translational Stroke Research / Issue 3/2011
Print ISSN: 1868-4483
Electronic ISSN: 1868-601X
DOI
https://doi.org/10.1007/s12975-011-0087-z

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