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 of species specificity of GABAA receptor function, further potentiating the importance of human neuronal models in understanding the synaptic role of alcohol. Alcohol’s impact on GABAA receptor function seems to be quite complex, and the sensitivity of receptor response to alcohol could be a key determinant of the type of effect seen. Receptor subunit stoichiometry and regulation of subunit expression in response to chronic alcohol exposure are believed to influence addiction characteristics, such as alcohol withdrawal and tolerance (Olsen & Sieghart, 2009). Work performed in both in vivo animal models and in vitro cultured animal cells revealed that chronic alcohol exposure does in fact change GABAA receptor subunit gene expression (Cagetti, Liang, Spigelman, & Olsen, 2003; L. L. Devaud, Smith, Grayson, & Morrow, 1995), specifically an increase in GABAA α4 (GABRA4) subunit and a decrease in expression of the α1 (GABRA1) subunit. Furthermore, studies performed using post-mortem human brain tissue found variations in γ2 (GABRG2) (Enoch et al., 2012) and
