We next explored the effects of acute alcohol exposure on the NMDA response, which in other model systems was attenuated by acute exposure to alcohol (Nie et al., 1994, Puglia and Valenzuela, 2010). In iPS-generated neurons, an acute exposure to 50mM alcohol significantly attenuated the peak amplitude of NMDA responses (p=0.036, Figure 3C). To further explore the use of human iPS-derived neural cells as a model to examine the effects of alcohol exposure, we explored whether tolerance to acute alcohol exposure could be observed in the culture after chronic alcohol treatment. Neural cultures were treated daily with 50mM alcohol for 7 days and alcohol withdrawn for 1 hr following transfer of coverslips to the recording chamber, and the acute effects of alcohol were measured. In neurons exposed to alcohol for 7 days, re-exposure to 50mM alcohol did not attenuate the NMDA response (p=0.77, Figure 3D). In contrast to results for NMDA receptors, no significant changes were observed following acute 50 mM alcohol exposure for GABAA (n=4, p=0.27, data not shown) or AMPA receptors (n=5, p=0.19, data not shown). As we
