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Striatal Sensitivity During Reward Processing in Attention-Deficit/Hyperactivity Disorder – Corrected Proof

Objective:
Attention-deficit/hyperactivity disorder (ADHD) has been linked to deficits in the dopaminergic reward-processing circuitry; yet, existing evidence is limited, and the influence of genetic variation affecting dopamine signaling remains unknown. We investigated striatal responsivity to rewards in ADHD combined type (ADHD-CT) using functional magnetic resonance imaging (fMRI), and whether it is modulated by variation in the dopamine transporter gene (DAT1).

Method:
We tested 29 male adolescents with ADHD-CT and 30 age-, handedness-, and gender-matched healthy controls who were selected for DAT110/6 haplotype dosage. Based on previous research, we focused our analysis on the ventral striatum and the caudate nucleus.

Results:
Three main findings emerged. First, male adolescents with ADHD-CT did not differ from controls in terms of blood oxygen–level dependent (BOLD) fMRI response to reward-predicting cues (gain or loss-avoidance) in the ventral striatum. Second, male adolescents with ADHD-CT showed a relative increase, compared with controls, in the striatal BOLD response to successful outcomes. Third, DAT110/6 dosage differentially modulated neural activation to reward-predicting cues in the caudate nucleus in the ADHD-CT and control groups.

Conclusions:
The findings challenge the idea of a deficit in anticipation-related activation in the ventral striatum in male adolescents with ADHD-CT, while suggesting that the processing of reward outcomes is dysfunctional, consistent with a recent neurobiological model of the disorder. Preliminary evidence suggests that polymorphic variations in genes affecting dopamine signaling need to be taken into consideration when investigating reward-related deficits in ADHD-CT.

Posted in: Journal Article Abstracts on 06/07/2012 | Link to this post on IFP |
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