Histone modifications including acetylation and deacetylation play a role in long-lasting changes in brain function associated with SUD. For example, brain region- and cell type-specific histone acteylation modification for gobal/genome-wide and promoter-specific changes have been reported for alcohol use. In particular, dysregulation of gene expression profiles across several brain regions are associated with exposure to alcohol, which is expected to contribute to the development of withdrawal symptoms (Mons & Beracochea, 2016). Similarly, cocaine administration was associated with elevated global histone acetylation levels in reward-related regions (i.e., nucleus accumbens) (Renthal et al., 2009). Consequently, histone modifications are likely to coordinate networks of brain structures to regulate symptoms of drug dependence and withdrawal.
