phosphorylation of GABAA receptor subunits reduced the binding of receptors with AP-2 and subsequent internalization (Kittler et al. 2008). Moreover, reduced PKC-dependent GABAA receptor phosphorylation increases receptor binding to the AP-2 and promotes receptor endocytosis (Terunuma et al. 2008). Chronic activation of PKA in cerebellar granule cells increases cell surface expression of GABAA receptor α1 subunit (Ives et al. 2002). EtOH exposure alters expression and translocation of PKA (Diamond and Gordon 1994; Newton and Messing 2006) suggesting that PKA is likely also involved in the trafficking of GABAA receptors following EtOH exposure. Future studies will determine the specific role of various protein kinases in GABAA receptor trafficking following chronic EtOH administration.
