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 receptors influence their functional and pharmacological properties (Olsen and Sieghart 2009), the changes in subunit expression following chronic alcohol exposure are thought to restore excitatory/inhibitory balance. In in vivo and in vitro rodent studies, chronic alcohol exposure increased the expression of the GABAA α4 subunit and decreased the expression of the α1 subunit (Devaud et al. 1995, Cagetti et al. 2003), a switch that reduces the chloride current passing through exogenously expressed GABAA receptors in mammalian cells (Picton and Fisher 2007), consistent with a compensatory response to alcohol’s potentiation of inhibitory transmission. Studies examining post mortem human brain samples from alcoholics and controls have reported differences in expression of the γ2 (Enoch et al. 2012) and δ subunits (Bhandage et al. 2014), although observed differences in expression may be limited to specific brain regions (Jin et al. 2012, Jin et al. 2014).
