Electrophysiological recordings from rodents provides evidence for potentiating effects of alcohol on postsynaptic GABAA receptor activity in neurons located in the cortex and hippocampus (Aguayo 1990, Weiner et al. 1994), amygdala (Nie et al. 2004), nucleus accumbens (Nie et al. 2000), and the retina (Yeh and Kolb 1997), although subsequent research has yielded variable findings including no effect (Criswell et al. 2003) or an attenuating effect (Xie et al. 2013) of alcohol, suggesting that alcohol’s actions at these receptors are complex. The GABAA receptor’s sensitivity to alcohol may be dependent on subunit stoichiometry (Sundstrom-Poromaa et al. 2002, Wei et al. 2004, Wallner et al. 2006), and molecular adaptations that regulate subunit expression in response to prolonged alcohol exposure are thought to contribute to alcohol tolerance and withdrawal. In rodent models, chronic alcohol exposure produced changes in GABAA subunit gene expression that varied with the length of alcohol exposure, duration of the withdrawal period, and the brain region examined (Mhatre and Ticku 1992, Mhatre and Ticku 1994, Devaud et al. 1995, Kumar et al. 2009). Because the subunit composition of GABAA
