Ethanol, the most commonly abused drug in humans easily passes the blood-brain barrier and interferes with brain function and behavior. Acute ethanol intoxication may present with symptoms of impaired mental and physical abilities at the blood concentrations >0.25% (~54 mM). Ethanol inhibits the NMDA-type glutamate receptor (NMDAR) (Peoples et al., 1997; Ferrani-Kile et al., 2003) and enhances GABAergic synaptic inhibition (Ariwodola and Weiner, 2004), which causes an imbalance of excitation and inhibition within the neuronal network, which may affect network properties such as γ oscillations. Indeed, ethanol at a moderate dose (0.8 g/kg, ~16 mM) alters stimulus-evoked γ oscillations in the human visual cortex and motor cortex (Campbell et al., 2014). Furthermore, ethanol withdrawal induces a rebound facilitation of γ oscillations in the rat cortex (Cheaha et al., 2014). However, it is not clear whether ethanol modulates γ oscillations at the local network level and, if so, by which the cellular mechanisms.
