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Role of Basal Ganglia in Sleep–Wake Regulation: Neural Circuitry and Clinical Significance

机译:基底神经节在睡眠-唤醒调节中的作用:神经回路和临床意义

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摘要

Researchers over the last decade have made substantial progress toward understanding the roles of dopamine and the basal ganglia (BG) in the control of sleep–wake behavior. In this review, we outline recent advancements regarding dopaminergic modulation of sleep through the BG and extra-BG sites. Our main hypothesis is that dopamine promotes sleep by its action on the D2 receptors in the BG and promotes wakefulness by its action on D1 and D2 receptors in the extra-BG sites. This hypothesis implicates dopamine depletion in the BG (such as in Parkinson's disease) in causing frequent nighttime arousal and overall insomnia. Furthermore, the arousal effects of psychostimulants (methamphetamine, cocaine, and modafinil) may be linked to the ventral periaquductal gray (vPAG) dopaminergic circuitry targeting the extra-BG sleep–wake network.
机译:在过去的十年中,研究人员在了解多巴胺和基底神经节(BG)在控制睡眠/苏醒行为中的作用方面取得了实质性进展。在这篇综述中,我们概述了有关通过BG和额外BG部位进行睡眠的多巴胺能调节的最新进展。我们的主要假设是,多巴胺通过其对BG中D2受体的作用促进睡眠,并通过其对BG外部部位D1和D2受体的作用促进觉醒。该假设暗示BG中多巴胺的消耗(例如帕金森氏病)会引起夜间频繁的觉醒和整体失眠。此外,精神刺激药(甲基苯丙胺,可卡因和莫达非尼)的刺激作用可能与靶向超BG睡眠-唤醒网络的腹周导水管灰色(vPAG)多巴胺能回路有关。

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