The DLPFC, while not studied as intensively as other prefrontal regions in relation to reward or in populations with alcohol dependence, has emerged as an important region in addiction. Altered DLPFC function in addiction is thought to reflect disrupted decision-making away from flexible responding and in favor of compulsive behavior [6], [39]. In addition, DLPFC is postulated to play a critical role in the self-regulation of reward consumption, for example by modulating the processing of reward value in the service of goals [40], [41], [42]. Alcohol-dependent adults exhibit reduced DLPFC response to cognitive control [43], and those with greater DLPFC response report greater craving [43] and are more likely to seek treatment [44]. Previous studies of alcohol use disorder have indicated that greater negative functional connectivity between the ventral striatum and DLPFC during operant conditioning is associated with slower learning from reward prediction errors and greater craving [45]. While our task involves other aspects of reward processing rather than learning, our findings could suggest a similar alteration of prefrontal influence over reward processing. That is, instead of reduced prefrontal influence
