Across conceptual models, disrupted function in neural reward circuitry is postulated to be a central mechanism of alcohol dependence and other forms of addiction [1], [2], [3]. Changes in reward circuitry with the development of addiction are thought to reflect a shift from reward-driven behavior during the initial stages of addiction to loss of reward function by later stages [4]. Recent models of addiction have focused on altered function in prefrontal regions that mediate behavioral processes such as compulsivity, impulsivity, and higher-order cognitive control [5], [6]. Together, these constructs reflect difficulty in controlling behavior flexibly, as directed by future goals rather than short-term gains, and through inhibition of inappropriate or goal-inconsistent behaviors, respectively. Specifically, adaptations related to the development of addiction are posited to involve increased hypofrontality, which can be conceptualized as poor executive control over behavior, as well as poor modulation of responding in other reward regions. In terms of prefrontal function, these adaptations are likely to involve altered function in regions such as the orbitofrontal cortex (OFC), medial prefrontal cortex (mPFC), and dorsolateral prefrontal cortex (DLPFC), all of
