Accumulating evidence suggests that GABA is a major player in dictating many of the behavioral effects of alcohol, including anxiolysis, motor incoordination, sedation, withdrawal phenotypes and alcohol preference (Lieberman et al., 2012). The associations between GABAA and alcohol were first speculated due to the parallels between the behavioral effects of alcohol and allosteric modulators of GABAA (barbiturates and benzodiazepines) (Grobin et al., 1998; Kumar et al., 2009; Weiner & Valenzuela, 2006). In addition, data from animal models suggest that the behavioral phenotypes of acute alcohol exposure can be influenced by co-application of GABAA agonists or antagonists. Electrophysiological recordings in several brain regions, from animal models, show 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 conducted using human iPS cell-derived neuronal cells contradict findings obtained from animal models (Lieberman et al., 2017). There was no observed strengthening of the GABAA response following acute exposure to alcohol (50 mM) (Lieberman et al., 2012). This is highly suggestive
