The neurodevelopmental implications of alcohol drinking during the adolescent period are becoming a cause for great concern warranting a greater understanding of these brain adaptations and how they affect the progression of alcoholism later in life (Guerri & Pascual, 2010; Spear, 2011). Epigenetic regulation of critical neural pathways has been recognized as a major effector in mediating these changes in neuroplasticity. Intermittent ethanol treatment of adolescent Wistar rats has been shown to increase histone H3K9 and H4K12 acetylation in the frontal cortex and NAc with a concomitant decrease in the striatum. However, these alterations in histone acetylation due to intermittent ethanol exposure were not preserved in adult rats further highlighting the vulnerability of the adolescent brain to binge-like alcohol drinking, the most common pattern of drinking among adolescents (Pascual, Boix, Felipo, & Guerri, 2009). In a subsequent study, Pascual et 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
