Our observations may also provide cues for therapies preventing ethanol withdrawal symptoms. Ethanol withdrawal can cause delirium tremens, characterized by hallucinations or even seizures. Withdrawal of ethanol after chronic use causes a strong increase in γ oscillations in rats (Cheaha et al., 2014). Enhanced γ oscillations are associated with psychosis (Hirano et al., 2015) and can even trigger seizures (de Curtis and Avoli, 2016). Withdrawal-induced increase in γ oscillations could be explained by a rebound effect caused by an adaptation to a chronic suppression of γ-generating networks. In theory, a temporary suppression of γ oscillations during ethanol withdrawal, e.g., by facilitation of the Akt/GSK3β signaling or NMDAR antagonists may alleviate withdrawal symptoms. Interestingly, increasing serotonin availability with fluoxetine reduced the withdrawal-induced γ oscillation rebound (Cheaha et al., 2014) and withdrawal symptoms in rats (Uzbay et al., 2004). Furthermore, the NMDAR antagonist ketamine was shown to be beneficial in the treatment of ethanol withdrawal symptoms (Wong et al., 2015).
