Strengths of the current study include its novel examination of acute and chronic effects of alcohol on the GABAA receptor in human neural cells in vitro and the examination of iPSC-derived neural cell lines from a cohort of 11 control and 13 alcoholic donor subjects. Our findings should be considered in light of several limitations, including that GABA-mediated currents were evoked via puff application of GABA with the micropipette targeted at the cell soma, which allowed us to examine only the postsynaptic effects of alcohol on primarily somatic GABAA receptor function. Presynaptic actions of alcohol have been reported, including increased the frequency of spontaneous inhibitory events (Sanna et al. 2004, Zhu and Lovinger 2006, Criswell et al. 2008) and increasing the amount of GABA released from presynaptic terminals (Nie et al. 2004). The presynaptic effects of alcohol may be mediated though actions on metabotropic glutamate and GABAB receptors (Nie et al. 2000, Zhu and Lovinger 2006). By exogenously applying GABA to evoke a current, we could examine only postsynaptic GABAA receptor function. Future studies using iPSC-derived neurons could extend our
