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Previous Article | Next Article
The Journal of Neuroscience, October 1, 2002, 22(19):8422-8428
Altered Histone Acetylation at Glutamate Receptor 2 and Brain-Derived Neurotrophic Factor Genes Is an Early Event Triggered by Status Epilepticus
Yunfei Huang, James J. Doherty, and Ray Dingledine Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia 30322
The mechanisms underlying seizure-induced changes in gene expression are unclear. Using a chromatin immunoprecipitation assay, we found that acetylation of histone H4 in rat hippocampal CA3 neurons was reduced at the glutamate receptor 2 (GluR2; GRIA2) glutamate receptor promoter but increased at brain-derived neurotrophic factor promoter P2 as soon as 3 hr after induction of status epilepticus by pilocarpine. This result indicates that status epilepticus rapidly activates different signal pathways to modulate histone acetylation in a promoter-specific manner. H4 deacetylation preceded seizure-induced GluR2 mRNA downregulation. The histone deacetylase inhibitor trichostatin A prevented and quickly reversed deacetylation of GluR2-associated histones. Trichostatin A also blunted seizure-induced downregulation of GluR2 mRNA in CA3. Thus, rapid gene-specific changes in histone acetylation patterns may be a key early step in the pathological processes triggered by status epilepticus.
Key words: BDNF; histone deacetylase; histone acetyltransferase; hippocampus; seizure; gene expression; glutamate; neurodegeneration; neuroprotection; GluR2; GRIA2
Copyright © 2002 Society for Neuroscience 0270-6474/02/22198422-07$05.00/0
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