Animal models have shown GIRK channels are important effectors in both opioid- and ethanol-induced analgesia (Ikeda et al. 2002), as well as being directly activated by ethanol with the involvement of a discrete alcohol pocket (Aryal et al. 2009). Another study on rat midbrain dopaminergic neurons suggests that the action of ethanol occurs on activated GIRK channels downstream of the GABAB receptors (Federici et al. 2009). The authors suggest that the enhancing effects of ethanol on GABAB responses could modulate alcohol intake and the mental and motor performance in an acute intoxicative phase. These receptors are the focus for developing new analgesics (Lotsch & Geisslinger 2011) or therapeutic compounds that could mitigate the effects of alcohol. Hence, this may also be a pathway by which alcohol can modulate oscillatory brain activity.
