In addition, adaptations in dopamine-system function are postulated to disrupt the functional connectivity of these prefrontal regions with the ventral striatum (VS), especially the nucleus accumbens. For example, in a positron emission tomography study, Volkow and colleagues reported that controls—but not alcohol-dependent adults—exhibited an association between decreased glucose metabolism in the OFC and increased methylphenidate-induced dopamine release in the VS [12]. This finding suggests altered coupling between these two regions, with an association between lower response in the OFC and increased dopamine in the VS, which could indicate less effective regulation of VS responding by OFC. Furthermore, in detoxified alcohol-dependent adults, weaker OFC functional connectivity with the midbrain predicts the likelihood of relapse [13]. Similarly, this finding raises the possibility that poor or suboptimal connectivity between OFC and basic reward regions is a correlate or consequence of addiction. Given the role of the OFC in inhibitory control and self-regulation [14], [15], these findings suggest that alcohol dependence involves reduced inhibition of ventral striatal response, which is relevant to compulsive use.
