D2 receptor binding was decreased following ethanol exposure or intake and withdrawal in rat, and this effect appeared to be larger in DS compared to NAc (Muller, Britton et al. 1980, Rommelspacher, Raeder et al. 1992). However, other studies found no change or increases in D2 receptor binding, and/or changes in D1 receptor binding following ethanol intake (Pellegrino and Druse 1992, De Montis, Gambarana et al. 1993, Lograno, Matteo et al. 1993, Kim, Lee et al. 1997, Souza-Formigoni, De Lucca et al. 1999). These differences could be due to numerous factors, including dose and duration of ethanol intake, timing of the assay relative to drinking/withdrawal, and which striatal subregion was examined. Altered D2 receptor occupancy has also been reported in humans with alcohol use disorders, with decreased receptor availability and negative correlation with craving being the most common findings (Ebert, Klein et al. 2002, Volkow, Wang et al. 2002, Heinz, Siessmeier et al. 2004, Heinz, Siessmeier et al. 2005, Watanabe, Kato et al. 2008, Rominger, Cumming et al. 2012). Stimulation of cAMP levels by D1 agonist is enhanced in DS slices, but not NAc, in ethanol-drinking rats (Nestby, Vanderschuren et al. 1999).
