Alcohol potentiates GABAA receptor-mediated responses and enhances inhibitory neurotransmission. Alterations in GABAergic signaling have been hypothesized to underlie all three stages of addiction. The rewarding properties of alcohol were hypothesized to depend on GABAA signaling in the nucleus accumbens and amygdala (Koob and Volkow, 2010; Volkow et al., 2016). Blockade of dopamine and GABAA receptors in the ventral pallidum prevents the reinforcing effects of alcohol (Koob and Volkow, 2010; Volkow et al., 2016). GABAergic signaling has also been implicated in increasing withdrawal-induced anxiety (Leung et al., 2015; Smith et al., 1998). Furthermore, neurocircuitry changes associated with drug- and cue-induced reinstatement after extinction have been linked to GABAergic projections from the nucleus accumbens to the ventral pallidum (Kalivas and O’Brien, 2008).
