In response to acute 40 mM ethanol application, we observed a significant increase in sIPSCs, which was accompanied by a decrease in sAP frequency, more prominently in MOR N40 AD-iNs. Next, we aimed to investigate the synaptic output of MOR N40D AD-iNs by monitoring miniature inhibitory postsynaptic currents (mIPSCs) in response to acute 40 mM ethanol application (Fig. 4). We found that acute ethanol application more robustly increased mIPSC frequency (Fig. 4A–C) in N40 versus D40 AD-iN cells, with no change in mIPSC amplitude (Fig. 4A, D). The frequency increase observed following ethanol application in N40 AD-iNs was significantly different when compared to D40 AD-iNs (Fig. 4C, *p ≤ 0.05). Furthermore, there was no significant difference in baseline mIPSC frequency between N40 and D40 iNs (Fig. 4E). We also measured the mIPSC kinetics and observed no differences in the average mIPSC rise time (Fig. 4F) and decay time (Fig. 4G) between MOR N40 and D40 AD-iNs before or after acute ethanol application. These data suggest an ethanol-mediated increase in synaptic release in N40 AD-iNs, ultimately indicating a presynaptic effect. Taken
