al demonstrated that the effects of ethanol on histone acetylation in the prefrontal cortex at specific gene promoters (cFos, Cdk5, FOSB and BDNF) and their potentiation through HDAC inhibition are associated with ethanol-induced conditioned place aversion and reinstatement (Pascual et al., 2012). Recently, we observed that acute ethanol inhibits HDAC and DNMT activities in the amygdala and only DNMT activity in the bed nucleus of stria terminalis of adolescent rats and produces anxiolytic-like effects (Sakharkar, Tang, et al., 2014). Adolescent rats, unlike adult rats, do not show the development of rapid tolerance to ethanol-induced anxiolysis and inhibition of HDAC in the amygdala (Sakharkar et al., 2012; Sakharkar, Tang, et al., 2014). Because the age of first alcohol exposure is believed to be an important predictor of increased risk of alcohol abuse, these studies necessitate further investigation to identify possible epigenetic marks or mechanisms involved in psychiatric and substance abuse disorders associated with adolescent alcohol exposure (DeWit, Adlaf, Offord, & Ogborne, 2000; Hawkins et al., 1997).
