Studies reporting alcohol modulation of GIRK channels have been well-documented (for a recent review, see Bodhinathan and Slesinger, 2014). KCNJ6/GIRK2 has also been found to be involved in addictions to several drugs, such as opioid/opiate (Lotsch et al., 2010), nicotine (Saccone et al., 2007; Nishizawa et al., 2014), morphine (Cruz et al., 2008), and cocaine (Morgan et al., 2003; Munoz and Slesinger, 2014). It is proposed that the regulator of G-protein signaling (RGS) proteins in the reward pathway might underlie adaptation to alcohol and other addictive drugs (Lomazzi et al., 2008). Neurochemical mechanisms underlying ethanol activation of GIRK channels have also been extensively studied (for reviews, see Luscher and Slesinger, 2010; Bodhinathan and Slesinger, 2014). It has been shown that mice lacking GIRK2 channels consumed more ethanol and failed to develop conditioned place preference for ethanol when compared to their controls (Blednov et al., 2001; Hill et al., 2003), suggesting that GIRK2 may be mediating the reinforcing and/or aversive motivational aspects of ethanol action. In a GWAS in the COGA sample with a neurophysiological phenotype (ERO theta power to targets
