Neuronal activity reorganization in motor cortex for successful locomotion after a lesion in the ventrolateral thalamus

Neuronal activity reorganization in motor cortex for successful locomotion after a lesion in the ventrolateral thalamus
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运动皮层神经元活动重组以实现腹外侧丘脑损伤后成功运动

DOI:
10.1152/jn.00191.2021
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发表时间:
2022
影响因子:
2.5
通讯作者:
Beloozerova, Irina N.
Beloozerova, Irina N.
中科院分区:
医学3区
文献类型:
--
作者:
Beloozerova, Irina N.

文献摘要

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如果接受小脑的腹外侧丘脑(VL)受到影响,则丘脑中风会导致共济失调。这种缺陷的补偿机制还不清楚,特别是单个神经元和丘脑外的特定神经元亚群在恢复中发挥的作用。本研究的目的是阐明运动过程中,当VL部分失活或损伤时,运动皮层参与缓解共济失调的神经机制。在自由走动的猫,我们记录了在运动皮层的V层神经元的活动,猫走在一个平面上,水平放置的梯子。我们首先可逆地灭活10%的VL单方面使用神经递质传递拮抗剂CNQX和分析如何重组运动皮层的活动,以支持成功的运动。接下来,我们使用红藻氨酸双侧损伤50%-75%的VL,并分析运动恢复时运动皮层的活动如何重组。当VL的一小部分失活时,运动皮层神经元的放电率下降,但其他活动接近正常,猫走得相当好。个别神经元保留了他们的能力,以响应需求的准确性在阶梯运动;然而,大多数改变了他们的反应。当VL被损毁时,猫在平坦表面上正常行走,但在损伤后的几天内在梯子上共济失调。当梯子运动正常化时,梯子上的神经元放电率是正常的,并且与肩部相关的组在步幅的摆动阶段优先活跃。新&值得注意的是,这是第一次分析与肩部、肘部或手腕相关的单个神经元和神经元亚群的活动重组,以及在丘脑中失活或损伤之前和之后行走的动物的运动皮层中的快传导和慢传导锥体束神经元。这些结果为丘脑卒中后自发恢复的机制提供了独特的见解,可能为缓解卒中后运动缺陷的新策略提供指导。
Thalamic stroke leads to ataxia if the cerebellum-receiving ventrolateral thalamus (VL) is affected. The compensation mechanisms for this deficit are not well understood, particularly the roles that single neurons and specific neuronal subpopulations outside the thalamus play in recovery. The goal of this study was to clarify neuronal mechanisms of the motor cortex involved in mitigation of ataxia during locomotion when part of the VL is inactivated or lesioned. In freely ambulating cats, we recorded the activity of neurons in layer V of the motor cortex as the cats walked on a flat surface and horizontally placed ladder. We first reversibly inactivated ∼10% of the VL unilaterally using glutamatergic transmission antagonist CNQX and analyzed how the activity of motor cortex reorganized to support successful locomotion. We next lesioned 50%–75% of the VL bilaterally using kainic acid and analyzed how the activity of motor cortex reorganized when locomotion recovered. When a small part of the VL was inactivated, the discharge rates of motor cortex neurons decreased, but otherwise the activity was near normal, and the cats walked fairly well. Individual neurons retained their ability to respond to the demand for accuracy during ladder locomotion; however, most changed their response. When the VL was lesioned, the cat walked normally on the flat surface but was ataxic on the ladder for several days after lesion. When ladder locomotion normalized, neuronal discharge rates on the ladder were normal, and the shoulder-related group was preferentially active during the stride’s swing phase.NEW & NOTEWORTHYThis is the first analysis of reorganization of the activity of single neurons and subpopulations of neurons related to the shoulder, elbow, or wrist, as well as fast- and slow-conducting pyramidal tract neurons in the motor cortex of animals walking before and after inactivation or lesion in the thalamus. The results offer unique insights into the mechanisms of spontaneous recovery after thalamic stroke, potentially providing guidance for new strategies to alleviate locomotor deficits after stroke.