Our data showed a clear picture of reduction of γ power when the concentration of ethanol was ≥25 mM. At intoxicating levels ethanol impairs working memory and perception amongst others (Schweizer et al., 2006), which can be explained by the strong suppression of γ oscillations reported here. Because ethanol even at intoxicated concentration also increases GABAA receptor mediated IPSCs (Wan et al., 1996; Wu et al., 2005; Zheng et al., 2016), it remains the question how an ethanol-induced increase in IPSCs would suppress γ oscillations. Ethanol could inhibit the activation or reduce excitatory drive of interneurons by pyramidal cells, since acute ethanol dose-dependently inhibits synaptic transmission (Hendricson et al., 2004; Badanich et al., 2013). Alternatively, ethanol could reduce interneuron excitability due to an increase of tonic inhibition (Wei et al., 2004), resulting from synaptic spillover acting on δ subunit-containing GABAA receptors (Mann and Mody, 2010). It seems that ethanol may enhance GABAergic neurotransmission via increment of interneuron excitability and GABA release, and may decrease glutamatergic neurotransmission via reduction of glutamate release(Hendricson et al., 2004) and inhibition of NMDA receptor function(Lovinger
