Abstract:
To improve the initiation and speed of intended action, one of the crucial mechanisms is suppressing unwanted movements that interfere with goal-directed behavior, which is observed relatively aberrant in Parkinson\'s disease patients. Recent research has highlighted that dopamine deficits in Parkinson\'s disease predominantly occur in the caudal lateral part of the substantia nigra pars compacta (SNc) in human patients. We previously found two parallel circuits within the basal ganglia, primarily divided into circuits mediated by the rostral medial part and caudal lateral part of the SNc dopamine neurons. We have further discovered that the indirect pathway in caudal basal ganglia circuits, facilitated by the caudal lateral part of the SNc dopamine neurons, plays a critical role in suppressing unnecessary involuntary movements when animals perform voluntary goal-directed actions. We thus explored recent research in humans and non-human primates focusing on the distinct functions and networks of the caudal lateral part of the SNc dopamine neurons to elucidate the mechanisms involved in the impairment of suppressing involuntary movements in Parkinson\'s disease patients.
摘要:
为了提高预期行动的启动和速度,关键机制之一是抑制干扰目标导向行为的不必要运动,在帕金森病患者中观察到相对异常。最近的研究表明,帕金森病的多巴胺缺陷主要发生在人类患者的黑质致密部(SNc)的尾外侧部分。我们之前在基底神经节内发现了两个平行回路,主要分为由SNc多巴胺神经元的延髓内侧部分和尾外侧部分介导的回路。我们进一步发现,在尾基底节回路的间接途径,由SNc多巴胺神经元的尾外侧部分促进,当动物进行自愿的目标指导行动时,在抑制不必要的非自主运动中起着关键作用。因此,我们探索了人类和非人类灵长类动物的最新研究,重点是SNc多巴胺神经元尾外侧部分的不同功能和网络,以阐明帕金森病患者抑制不自主运动的损害机制。