Phosphatidylinositol-3 kinase (PI3K) converts phosphatidylinositol (3,4)-bisphosphate (PIP2) to phosphatidylinositol (3,4,5)-trisphosphate (PIP3) in the plasma membrane (Yuan and Cantley, 2008), and is involved in many neuronal functions, including neuronal plasticity (Karpova et al., 2006). Wortmannin, a potent and highly selective inhibitor of PI3-kinase had no effect on control γ power (104.3 ± 6.5% of baseline, n.s.) nor ethanol-induced suppression of γ (Figures 4A,B). On average, in the presence of wortmannin (200 nM), 50 mM ethanol caused a 38.7 ± 6.9% decrease (P < 0.05, vs. wortmannin baseline, n = 8), which was not different from that of 50 mM ethanol alone (Student t-test, P > 0.05, Figures 4A,B). The reduction induced by 100 mM ethanol in the presence of wortmannin was 63.5 ± 4.7% (P < 0.01 vs. wortmannin baseline, n = 8, Figure 4B), which was not different from that of 100 mM ethanol alone (Student t-test, P > 0.05, Figure 4B). These results suggest that PI3 kinase activation was not involved in the ethanol-induced suppression of γ oscillations.
