Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School Boston, MA, USA.
Front Neuroanat. 2010 Nov 23;4:145. doi: 10.3389/fnana.2010.00145. eCollection 2010.
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.
在过去的十年中，研究人员在理解多巴胺和基底神经节（BG）在睡眠-觉醒行为控制中的作用方面取得了重大进展。在这篇综述中，我们概述了最近关于通过 BG 和 BG 外部位点的多巴胺调制来调节睡眠的进展。我们的主要假设是，多巴胺通过其在 BG 中的 D2 受体作用促进睡眠，并通过其在 BG 外部位点的 D1 和 D2 受体作用促进觉醒。这一假设表明，BG 中的多巴胺耗竭（如帕金森病）会导致夜间频繁觉醒和整体失眠。此外，精神兴奋剂（甲基苯丙胺、可卡因和莫达非尼）的觉醒作用可能与靶向 BG 外睡眠-觉醒网络的腹侧periaqueductal 灰色（vPAG）多巴胺能回路有关。
