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首页> 外文期刊>Journal of the American Academy of Child and Adolescent Psychiatry >Striatal sensitivity during reward processing in attention-deficit/ hyperactivity disorder
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Striatal sensitivity during reward processing in attention-deficit/ hyperactivity disorder

机译：注意缺陷/多动障碍奖赏过程中的纹状体敏感性

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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). We tested 29 male adolescents with ADHD-CT and 30 age-, handedness-, and gender-matched healthy controls who were selected for DAT1 10/6 haplotype dosage. Based on previous research, we focused our analysis on the ventral striatum and the caudate nucleus. 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, DAT1 10/6 dosage differentially modulated neural activation to reward-predicting cues in the caudate nucleus in the ADHD-CT and control groups. 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.
机译：注意缺陷/多动障碍（ADHD）与多巴胺能奖赏处理电路的缺陷有关。然而，现有证据有限，遗传变异影响多巴胺信号传导的影响仍然未知。我们使用功能磁共振成像（fMRI）研究了ADHD合并型（ADHD-CT）对奖励的纹状体反应性，以及是否受多巴胺转运蛋白基因（DAT1）的变化调节。我们测试了29位患有ADHD-CT的男性青少年和30位年龄，惯性和性别匹配的健康对照者，这些对照者被选择用于DAT1 10/6单倍剂量。基于先前的研究，我们将分析重点放在腹侧纹状体和尾状核。出现了三个主要发现。首先，患有ADHD-CT的男性青少年在对腹侧纹状体中奖励预测线索（增益或避免损失）的血氧水平依赖性（BOLD）fMRI反应方面与对照组没有差异。其次，与对照组相比，ADHD-CT男性青少年对成功结局的纹状体BOLD反应相对增加。第三，在ADHD-CT组和对照组中，DAT1 10/6剂量差异调节神经激活，以预测尾状核中的奖励线索。该发现挑战了ADHD-CT男性青少年腹侧纹状体预期相关激活不足的想法，同时表明奖励结果的处理功能失调，与该疾病的最新神经生物学模型一致。初步证据表明，在调查ADHD-CT中与奖赏相关的缺陷时，应考​​虑影响多巴胺信号传导的基因的多态性变异。

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