Rutgers Center for Molecular and Behavioral Neuroscience
Neurocognitive alterations to mesocorticolimbic reward function by drugs of abuse are thought to facilitate a progression towards excessive drug use. Despite efforts to identify methods to counteract such drug-induced neural alterations, brain-based treatments for this disorder remain underdeveloped and often ineffective. In this talk, I propose that the anterior cingulate cortex (ACC) putative function—selecting and motivating the execution of extended goal-directed behaviors—can be utilized as a biomarker for the abnormal reward processes underlying substance misuse. I will present support for this proposal utilizing the reward positivity as a quantifiable EEG metric of reward-related ACC function. First, people who abuse addictive substances produce a relatively small reward positivity to monetary incentives, and that this impairment is modulated by a genetic polymorphism that codes for the expression of dopamine D4 receptors. Second, drug rewards (puffs of a cigarette) elicit a relatively larger reward positivity than nondrug rewards (money) in abstinent smokers. Third, applying excitatory or inhibitory stimulation to a subject-specific frontal-cingulate reward pathway using robot-assisted fMRI-guided rTMS can alter the amplitude of the reward positivity elicited by drug and non-drug rewards. In sum, our efforts point to a decisive role of integrating multimodal neuroimaging methods as an early stage in treatment development for substance use disorders, with a highly sensitive EEG-based biomarker of addiction severity and treatment efficacy.