Clathrin and the adaptor complex (AP) play a crucial role in the internalization of GABAA receptors following chronic EtOH administration. Notably, in the intracellular fraction, the clathrin-α1-GABAA receptor complex is increased following chronic EtOH administration (Kumar et al. 2004). Specific GABAA receptor subunits (β2 and/or γ2) are required for recognition of the receptor by the AP-2 that precedes clathrin-dependent endocytosis (Herring et al. 2003; Kittler et al. 2008). Chronic EtOH exposure induces an increase in the expression of α4-, β2-, and β3- GABAA receptor subunits in the cerebral cortex and all of these subunits contain consensus phosphorylation sites for PKC. In contrast, α1, α2, and α3 GABAA receptor subunits are decreased in the cortex and these subunits do not contain consensus phosphorylation sites for PKC. Hence, it has been hypothesized that PKC may phosphorylate the GABAA receptor subunits and/or AP-2 following chronic EtOH administration, altering the recognition and endocytosis of GABAA receptors by blocking AP-2 binding (Macdonald 1995; Mohler et al. 1996). A single dose of EtOH also increases the internalization of GABAA receptor α4 and δ subunits (Liang et
