to the PFC where there was strong relationship between alcohol-induced decrease of H4 acetylation and long-lasting working memory impairments, H4 acetylation in the HPC (the CA1 region) was decreased in behaviorally “unimpaired” alcohol-treated mice and even continued to decrease in “impaired” withdrawal-treated mice, compared with water-treated mice (31, 47). However, the drugs that prevented alcohol’s effects in the PFC did not rescue alcohol’s effects on HPC function, underscoring a region-specific influence of regulatory epigenetic signature on adaptive processes that lead to alcohol tolerance and dependence.
