Phosphorylation of various GABAA receptor subunits can alter receptor function without altering receptor expression. We have shown that acute ethanol administration (2 g/kg) decreased serine phosphorylation of GABAA receptor β subunits without altering the expression of these subunits in the P2 fraction of rat cerebral cortex (Kumar et al. 2006). This suggests that ethanol may alter the phosphorylation state of receptors to alter GABAA receptor function and these effects may contribute to ethanol actions. This is consistent with the observation of increased GABAA receptor function following ethanol exposure. Likewise, reduced phosphorylation of the GABAA receptor γ2 subunit enhances the action of ethanol (Qi et al. 2007). PKCε phosphorylates the GABAA receptor γ2 subunit at serine327 in vitro and γ2 serine327 phosphorylation is reduced in mice lacking PKCε. In addition, exposure to ethanol (4 g/kg) for 1 h increases γ2 serine327 phosphorylation in the cerebellum of wildtype mice, but not PKCε knockout mice and this leads to reduced GABAA receptor function in cerebellar microsacs (Qi et al. 2007). Finally, phosphorylation at serine327 on GABAA receptor γ2 subunits is required for PKCε-mediated
