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• W1503830589 abstract "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." @default.
• W1503830589 created "2016-06-24" @default.
• W1503830589 creator A5034817273 @default.
• W1503830589 creator A5041248710 @default.
• W1503830589 creator A5054609222 @default.
• W1503830589 date "2002-10-01" @default.
• W1503830589 modified "2023-10-15" @default.
• W1503830589 title "Altered Histone Acetylation at<i>Glutamate Receptor 2</i>and<i>Brain-Derived Neurotrophic Factor</i>Genes Is an Early Event Triggered by Status Epilepticus" @default.
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• W1503830589 doi "https://doi.org/10.1523/jneurosci.22-19-08422.2002" @default.
• W1503830589 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6757766" @default.
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