With respect to mice, the DBA/2J (DBA) strain shows relatively low levels of voluntary ethanol consumption as compared to C57BL/6J (C57) mice. Microarray analysis has demonstrated very different patterns of gene activation in PFC of these two strains in response to acute alcohol exposure. DBA mice showed a greater change in the number of genes that were upregulated in response to EtOH than their C57 counterparts (Kerns et al., 2005). Among those transcripts upregulated were a number of genes that encode for glucocorticoid-binding proteins and cortisol levels are known to increase after acute alcohol consumption (King et al., 2006). This suggests that the divergent response in PFC gene expression between the two strains following ethanol challenge may indicate a differential response to circulating glucocorticoids. Other genes that were upregulated in the microarray study included those related to synaptic plasticity and 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
