of some of the neuroprotective genes downstream of CREB (Volakakis et al., 2010). Ppargc1a expression is also increased, and it is responsible for inducing another set of neuroprotective genes that respond to oxidative stress (Volakakis et al., 2010). The increased CREB signaling could in part be responding to oxidative or excitotoxic stress in these animals. The acumbens shell also showed increased CREB signaling in these animals, but the central amygdala did not (McBride et al., 2014). Chronic alcohol has been shown to decrease the phosphorylation of CREB, in other brain regions (Crews and Nixon, 2009). cAMP-mediated signaling was affected in both the acumbens shell and central amygdala of these animals(McBride et al., 2014). The overlap analysis with human data (Supplementary Table 1 & 5, Figure 2) suggests that cAMP and CREB signaling also play an important role in alcohol use disorders in humans.
