myelination. Interestingly, there was grouping of upregulated genes around specific chromosomal regions suggesting some common element that underlies ethanol-responsive genes. Chronic EtOH has been shown to alter the acetylation of histones (Pascual et al., 2009), so that chromatin rearrangement following ethanol exposure may play a role in these changes in gene expression. Alcohol-preferring AA rats show increased phosphorylation and subsequent inhibition of GSK-3β, involved in metabolism and possibly neurotransmission, in response to increased phosphorylation of AKT, a regulator of GSK-3β (Neznanova et al., 2009).
