3 and 4). The increase in the frequency of mIPSCs suggests that acute ethanol application impacts presynaptic GABAergic terminals in iNs expressing the MOR N40 genetic variant, with no effect on amplitude (Fig. 4). Finally, a CIE exposure paradigm for a duration of 10 days caused a significant increase in mIPSC frequency, exclusively in D40 AD-iN cells (Fig. 5). Our findings suggest that the exposure time and concentration for ethanol on AD-iNs (acute versus chronic; also 40 mM versus a maximum of 75 mM) confers differential sensitivity to synaptic output, which is dependent on the MOR genotype. These data will help elucidate the synaptic consequences of the N40D SNP, in response to ethanol, in human neurons.
