to clamp the AD-iNs at −70 mV rather than 0 mV. Spontaneous inhibitory postsynaptic currents (sIPSCs) were monitored for 5 min prior to ethanol application to measure the baseline responses in both N40 and D40 AD-iNs (Control, Fig. 3A). Following the addition of 40 mM ethanol, we observed a robust increase in the frequency of sIPSCs in MOR N40 AD-iNs, relative to controls. Interestingly, only a modest non-significant increase was observed in D40, relative to N40 AD-iNs (Fig. 3B and C). There were no changes observed for sIPSC amplitude in both genotypes tested (Fig. 3D). There were no significant differences observed in baseline sIPSC frequency between N40 and D40 AD-iNs (Fig. 3E). We next measured the sIPSC kinetics and observed no differences in the average sIPSC rise time (Fig. 3F) between genotypes before and after acute ethanol application. Interestingly, we observed a significant increase in the average sIPSC decay time prior to ethanol application (Fig. 3G, *p ≤ 0.05) between MOR N40 and D40 AD-iNs, and this difference was not detected following ethanol application. These data suggest that acute ethanol application results in an enhancement in network and/or synaptic activity in a relatively homogenous population of inhibitory N40 AD-iNs, suggesting
