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Reward, interrupted: Inhibitory control and its relevance to addictions

机译:奖励,被打断:抑制性控制及其与成瘾的关系

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There are broad individual differences in the ability to voluntarily and effortfully suppress motivated, reward-seeking behaviors, and this review presents the hypothesis that these individual differences are relevant to addictive disorders. On one hand, cumulative experience with drug abuse appears to alter the molecular, cellular and circuit mechanisms that mediate inhibitory abilities, leading to increasingly uncontrolled patterns of drug-seeking and -taking. On the other, native inter-individual differences in inhibitory control are apparently a risk factor for aspects of drug-reinforced responding and substance use disorders. In both cases, the behavioral manifestation of poor inhibitory abilities is linked to relatively low striatal dopamine D2-like receptor availability, and evidence is accumulating for a more direct contribution of striatopallidal neurons to cognitive control processes. Mechanistic research is now identifying genes upstream of dopamine transmission that mediate these relationships, as well as the involvement of other neurotransmitter systems, acting alone and in concert with dopamine. The reviewed research stands poised to identify new mechanisms that can be targeted by pharmacotherapies and/or by behavioral interventions that are designed to prevent or treat addictive behaviors and associated behavioral pathology. This article is part of a Special Issue entitled 'NIDA 40th Anniversary Issue'.
机译:在自愿和努力抑制动机,寻求奖励行为的能力方面存在广泛的个体差异,该综述提出了以下假设:这些个体差异与成瘾性疾病有关。一方面,吸毒的累积经验似乎改变了介导抑制能力的分子,细胞和回路机制,导致越来越多的不受控制的吸毒和吸毒模式。另一方面,抑制控制方面的天然个体间差异显然是药物强化反应和物质使用障碍方面的风险因素。在这两种情况下,抑制能力较差的行为表现都与纹状体多巴胺D2样受体相对较低有关,并且越来越多的证据表明纹状体外层神经元对认知控制过程有更直接的贡献。机理研究现在正在鉴定多巴胺传递上游的基因,这些基因介导这些关系,以及其他神经递质系统的参与,它们单独发挥作用并与多巴胺协同作用。这项经过审查的研究蓄势待发,可以确定药物治疗和/或旨在预防或治疗成瘾行为和相关行为病理学的行为干预所针对的新机制。本文是名为“ NIDA 40周年纪念日”的特刊的一部分。

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