A recent meta-analysis on the dopamine system and sedative drug use, including alcohol, suggests lower striatal D2/D3 receptor availability in alcohol users compared to healthy controls (Kamp et al., 2019). While acute alcohol may be related to modest increases in striatal DA release in social drinkers, in family history positive (FHP) and family history negative (FHN) individuals without AUD, and in AUD (Kegeles et al., 2018; Setiawan et al., 2014; Urban et al., 2010; Yoder et al., 2016), more chronic alcohol use results in dysfunctional DA transmission as evidenced by findings of lower amphetamine-induced increases in DA release in striatum in recently detoxified individuals with AUD vs. controls (Kamp et al., 2019). To date, few PET investigations have examined SG differences in dopaminergic alterations related to alcohol use or AUD. For example, using the D2/3 radiotracer [11C]raclopride, oral alcohol evoked significant ventral striatal DA release in young adult social drinkers (Urban et al., 2010). In this group, men had greater DA release than women in the ventral striatum in response to alcohol (men: ΔBPND = −12 ± 8%; women: ΔBPND
