Several studies have employed the use of patient-specific iPS cell technologies to model and elucidate the mechanisms underlying AUDs (reviewed by Prytkova, Goate, Hart, & Slesinger, 2018; Scarnati, Halikere, & Pang, 2019). Electrophysiological recordings conducted in several brain regions, from animal models, report a potentiation of GABAA receptor response following exposure to alcohol (Aguayo, 1990; Jia, Chandra, Homanics, & Harrison, 2008; Nie et al., 2004; Nie, Madamba, & Siggins, 2000; Yeh & Kolb, 1997). However, recordings performed in iPS cell-derived human neuronal cells contradict these findings (Lieberman, Kranzler, Levine, & Covault, 2017). However, these recordings were performed in mixed excitatory/inhibitory co-cultures, and a puffing procedure was used to specifically measure the effect of ethanol on postsynaptic GABAA receptors. There was no apparent strengthening of the GABAA response following acute exposure to alcohol. This suggests species-specific mechanisms governing GABAA receptor function, which supports the importance of human neuronal models in understanding the synaptic role of alcohol. Finally, the mechanisms of how GABAergic release and GABAA receptor function are impacted by alcohol application in human neurons carrying functionally important and commonly found
