A growing set of studies in both humans and animals have indicated that alcohol exposure causes widespread, dynamic changes of histone acetylation patterns, and thereby dysregulation in gene expression profiles across multiple brain regions (28, 124–126). Most of the studies have focused on the two histones H3 and H4 acetylation and chromatin-related events within the PFC, the HPC, and the AMG. In mouse and rat brain, studies reported that alcohol’s effects on histone acetylation patterns depend on the alcohol treatment paradigm, the timing of alcohol exposure or withdrawal, and brain structures examined, and even within a structure, alcohol can affect differently subregions. For example, work from Pandey’s lab has shown that anxiolytic-like responses caused by acute ethanol i.p. injection were accompanied by increased HAT CBP activity and associated increased acetylation of histone H3 at lysine 9 and histone H4 at lysine 8 (H3K9 and H4K8, respectively) leading to rapid elevation of NPY (mRNA and protein level) specifically in the central and medial, but not the basolateral amygdaloid, nuclei (125). The same group observed that a 2-week ethanol exposure followed by
