Essential Role of Histone Methyltransferase G9a in Rapid Tolerance to the Anxiolytic Effects of Ethanol
Author(s) -
Tiffani D.M. Berkel,
Huaibo Zhang,
Tara Teppen,
Amul J. Sakharkar,
Subhash C. Pandey
Publication year - 2018
Publication title -
the international journal of neuropsychopharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 107
eISSN - 1469-5111
pISSN - 1461-1457
DOI - 10.1093/ijnp/pyy102
Subject(s) - anxiolytic , histone deacetylase , ethanol , elevated plus maze , neuropeptide y receptor , neuropeptide , chemistry , endocrinology , pharmacology , amygdala , medicine , liquid diet , histone deacetylase inhibitor , biochemistry , histone , anxiety , psychiatry , receptor , gene
Tolerance to ethanol-induced anxiolysis promotes alcohol intake, thus contributing to alcohol use disorder development. Recent studies implicate histone deacetylase-mediated histone H3K9 deacetylation in regulating neuropeptide Y expression during rapid ethanol tolerance to the anxiolytic effects of ethanol. Furthermore, the histone methyltransferase, G9a, and G9a-mediated H3K9 dimethylation (H3K9me2) have recently emerged as regulators of addiction and anxiety; however, their role in rapid ethanol tolerance is unknown. Therefore, we investigated the role of G9a-mediated H3K9me2 in neuropeptide Y expression during rapid ethanol tolerance.
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