The drugs of abuse, including alcohol, exert and maintain their reinforcing effects through the reward circuitry of the brain [1,2]. Neuroimaging studies have documented the disruption of reward processing in addiction [3] and implicated brain reward circuitry in different stages of alcohol use disorder (AUD) [4]. The reward network, in the context of addiction, primarily includes structures from the midbrain (i.e., ventral tegmental area, VTA), basal ganglia (i.e., nucleus accumbens, NAc; caudate nucleus; and putamen), limbic system (i.e., amygdala, hippocampus, and thalamus), and cerebral cortical regions (i.e., prefrontal cortices, insula, cingular cortices, and superior and inferior parietal lobules) [1,2,5,6,7]. Deficient reward processing due to abnormalities in the reward network in individuals with chronic AUD has been widely reported for both monetary and drug-related rewards [8,9,10,11,12,13,14,15,16]. For instance, an fMRI finding reported by Wrase et al. [10] showed that the ventral striatum (VS), a key reward region, showed increased activation for alcohol-related cues, but decreased activation for monetary gain in detoxified alcoholics, relative to healthy controls, suggesting differential activation of VS in response to the type of reward. Both animal and
