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矛盾性运动障碍也许不再是一个需要等待 100 年才能解开的谜团。

Paradoxical kinesia may no longer be a paradox waiting for 100 years to be unraveled.

机构信息

Experimental and Biological Psychology, Behavioral Neuroscience, Faculty of Psychology, Philipps-University of Marburg, Gutenbergstraße 18, 35032 Marburg, Germany.

Marburg Center for Mind, Brain, and Behavior (MCMBB), Hans-Meerwein-Straße 6, 35032 Marburg, Germany.

出版信息

Rev Neurosci. 2023 Mar 20;34(7):775-799. doi: 10.1515/revneuro-2023-0010. Print 2023 Oct 26.

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder mainly characterized by bradykinesia and akinesia. Interestingly, these motor disabilities can depend on the patient emotional state. Disabled PD patients remain able to produce normal motor responses in the context of urgent or externally driven situations or even when exposed to appetitive cues such as music. To describe this phenomenon Souques coined the term "paradoxical kinesia" a century ago. Since then, the mechanisms underlying paradoxical kinesia are still unknown due to a paucity of valid animal models that replicate this phenomenon. To overcome this limitation, we established two animal models of paradoxical kinesia. Using these models, we investigated the neural mechanisms of paradoxical kinesia, with the results pointing to the inferior colliculus (IC) as a key structure. Intracollicular electrical deep brain stimulation, glutamatergic and GABAergic mechanisms may be involved in the elaboration of paradoxical kinesia. Since paradoxical kinesia might work by activation of some alternative pathway bypassing basal ganglia, we suggest the IC as a candidate to be part of this pathway.

摘要

帕金森病(PD)是一种进行性神经退行性疾病,主要表现为运动迟缓、运动不能。有趣的是,这些运动障碍可能取决于患者的情绪状态。运动障碍的 PD 患者在紧急或外部驱动的情况下,甚至在面对奖赏性提示(如音乐)时,仍能够产生正常的运动反应。一个世纪前,Souques 创造了“反常运动”一词来描述这种现象。此后,由于缺乏能够复制这种现象的有效动物模型,反常运动的机制仍不清楚。为了克服这一限制,我们建立了两种反常运动的动物模型。使用这些模型,我们研究了反常运动的神经机制,结果表明下丘(IC)是一个关键结构。脑深部电刺激、谷氨酸能和 GABA 能机制可能参与了反常运动的产生。由于反常运动可能通过激活绕过基底神经节的替代途径来发挥作用,我们认为 IC 可能是该途径的一部分。

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