Evidence supports the involvement of the ACB in mediating ethanol drinking (reviewed in Koob et al., 1998; McBride and Li, 1998). In particular, the shell portion of the ACB is involved in supporting reinforcement (Ikemoto et al., 1997) and reinforcing effects of drugs of abuse (reviewed in Kalivas et al., 1993). The central nucleus of the amygdala (CeA) has also been implicated in mediating the effects of ethanol (Koob and Le Moal, 2008; McBride, 2002) and dependence-induced alcohol drinking (Roberts et al., 1996). Therefore, changes in gene expression in the ACB-shell and CeA (2 regions that are part of the extended amygdala), following binge-like alcohol drinking that produces high BACs (> 80 mg%), were undertaken. In addition, time-course effects were also determined to better characterize ethanol-induced changes in gene expression following a drinking episode. The hypothesis to be tested was ‘binge-like’ alcohol drinking will produce differential changes in the expression of genes involved in synaptic function and intracellular signaling within the extended amygdala that will be time- and region- dependent.
