The serine/threonine kinase Akt is a major kinase of growth factor signaling, can be activated by PI3-kinase or by a PI3-kinase-independent mechanism such as cyclic AMP-dependent protein kinase A (Filippa et al., 1999) or dopamine (Brami-Cherrier et al., 2002). Acute ethanol exposure increases the phosphorylation of Akt (Carter et al., 2008; Zeng et al., 2012). We thus tested whether TCBN, a selective Akt inhibitor, affects the effect of ethanol on γ oscillations. TCBN (5 μM) caused a small increase in γ power (21.1 ± 6.7%, P < 0.05, vs. baseline, n = 16), but occluded the suppression of γ oscillations by ethanol (example in Figure 4C). The effect of ethanol (50 mM) in the presence of TCBN (16.1 ± 10.2%, P > 0.05 vs. TCBN baseline, n = 16) was smaller than that in the absence of TCBN (Student t-test, P < 0.001 vs. 50 mM ethanol alone, Figure 4D). Similarly, the effect of 100 mM ethanol in the presence of TCBN (3.1 ± 14.8%, P > 0.05 vs. TCBN baseline, n = 11) was smaller than that in the
