甲状腺下核和脊髓之间的相互作用控制着帕金森症的感知障碍
Keri-Ann Charles1,2, Elba Molpeceres Sierra1,2, Rabia Bouali-Benazzouz1,2
1Institut des Maladies Neurodégénératives, Université de Bordeaux, UMR 5293, F-33000 Bordeaux, France.
Brain : a journal of neurology
|June 25, 2024
概括
帕金森病的疼痛与下丘脑核 (STN) 功能障碍有关. STN深度大脑刺激 (DBS) 通过通过下降途径使脊髓活动正常化来减少疼痛,提供了一个新的治疗点.
科学领域:
- 神经科学是一个神经科学.
- 疼痛研究 疼痛研究
- 帕金森病病理生理病理学
背景情况:
- 疼痛是帕金森病 (PD) 的一个虚弱的非运动性症状.
- 基底质,特别是亚体质核 (STN) 中体感官处理的改变与PD相关的过敏相关.
- 将STN功能与疼痛联系在一起的确切机制仍未确定.
研究的目的:
- 研究STN与脊髓背部角 (DHSC) 在疼痛处理中的相互作用.
- 为了确定STN深度大脑刺激 (DBS) 对感觉处理的影响.
- 阐明在STN-DBS介导的止痛中,下降脑干通道和STN质神经元的作用.
主要方法:
- 利用了帕金森病的6-OHDA动物模型.
- 采用体内电生理学来记录STN和DHSC神经元,行为测试的 nociception,STN-DBS,和设计者受体专用激活的设计者药物 (DREADDs) 在STN.
- 通过使用Vglut2-ires-cre小鼠,专门抑制STN质神经元.
主要成果:
- STN神经元表现出 nociceptive 敏感性,强度编码,和风起类似的可塑性,镜像 DHSC 神经元.
- 这些功能在多巴胺缺乏的动物中受损,在STN和DHSC中强度反应发生变化.
- 在大鼠中,STN-DBS改善了全体运动,通过下降的大脑干路径调节,使DHSC神经活动正常化. 选择性抑制STN谷氨基神经元复制了这种止痛效应.
结论:
- 在帕金森病中,STN在 nociceptive 电路和疼痛感觉中起着至关重要的作用.
- STN-DBS通过通过下降的大脑干途径正常化脊柱WDR神经元反应来产生止痛作用.
- 治疗效果是通过抑制STN谷物质神经元来实现的.
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