Abstract
Cocaine addiction is characterized by impulsivity, impaired social relationships, and abnormal mesocorticolimbic reward processing, but their interrelationships relative to stages of cocaine addiction are unclear. We assessed blood-oxygenation-level dependent (BOLD) signal in ventral and dorsal striatum during functional magnetic resonance imaging (fMRI) in current (CCD; n = 30) and former (FCD; n = 28) cocaine dependent subjects as well as healthy control (HC; n = 31) subjects while playing an interactive competitive Domino game involving risk-taking and reward/punishment processing. Out-of-scanner impulsivity-related measures were also collected. Although both FCD and CCD subjects scored significantly higher on impulsivity-related measures than did HC subjects, only FCD subjects had differences in striatal activation, specifically showing hypoactivation during their response to gains versus losses in right dorsal caudate, a brain region linked to habituation, cocaine craving and addiction maintenance. Right caudate activity in FCD subjects also correlated negatively with impulsivity-related measures of self-reported compulsivity and sensitivity to reward. These findings suggest that remitted cocaine dependence is associated with striatal dysfunction during social reward processing in a manner linked to compulsivity and reward sensitivity measures. Future research should investigate the extent to which such differences might reflect underlying vulnerabilities linked to cocaine-using propensities (e.g., relapses).
Highlights
Deficits in impulse control and reward processing are hypothesized to initiate and sustain cocaine dependence [1,2,3,4], which is characterized by favoring immediate rewards of drug use over delayed non-drug rewards, despite potential negative consequences [5]
Mesocorticolimbic circuits, involving the dopaminergically innervated ventral and dorsal striatum as well as orbitofrontal and anterior cingulate cortices, are crucially involved in reward processing, and dysregulation in these circuits is implicated in both impulsivity and cocaine dependence [1,6,7,8,9,10]
One explanation for diminished mesocorticolimbic activation involves the rewarddeficiency syndrome (RDS) hypothesis [15], which conjectures that drugs of abuse, due to their potent dopaminergic effects, normalize ventral striatal dopamine levels, whereas non-drug related rewards fail to do so, leading RDS individuals to seek cocaine or other abused drugs
Summary
Deficits in impulse control and reward processing are hypothesized to initiate and sustain cocaine dependence [1,2,3,4], which is characterized by favoring immediate rewards of drug use over delayed non-drug rewards, despite potential negative consequences [5]. One explanation for diminished mesocorticolimbic activation involves the rewarddeficiency syndrome (RDS) hypothesis [15], which conjectures that drugs of abuse, due to their potent dopaminergic effects, normalize ventral striatal dopamine levels, whereas non-drug related rewards fail to do so, leading RDS individuals to seek cocaine or other abused drugs. Long-term, chronic cocaine abuse has been shown, to exacerbate underlying nondrug reward response deficiencies, through remodeling of neural circuitry [6,16,17,18]. This so-called ‘hijacking’ of the reward system leads abusers to attribute even greater value to drugrelated rewards at the expense of non-drug rewards [19,20]
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