Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Brain Res Bull. 2020 Jul;160:8-23. doi: 10.1016/j.brainresbull.2020.04.006. Epub 2020 Apr 13.
Constraint-induced movement therapy (CIMT) has proven to be an effective way to restore functional deficits following stroke in human and animal studies, but its underlying neural plasticity mechanism remains unknown. Accumulating evidence indicates that rehabilitation after stroke is closely associated with synaptic plasticity. We therefore investigated the impact of CIMT on synaptic plasticity in ipsilateral and contralateral brain of rats following stroke. Rats were subjected to 90 minutes of transient middle cerebral artery occlusion (MCAO). CIMT was performed from 7 days after stroke and lasted for two weeks. Modified Neurology Severity Score (mNSS) and the ladder rung walking task tests were conducted at 7,14 and 21 days after stroke. Golgi-Cox staining was used to observe the plasticity changes of dendrites and dendritic spines. The expression of glutamate receptors (GluR1, GluR2 and NR1) were examined by western blot. Our data suggest that the dendrites and dendritic spines are damaged to varying degrees in bilateral sensorimotor cortex and hippocampus after acute stroke. CIMT treatment enhances the plasticity of dendrites and dendritic spines in the ipsilateral and contralateral sensorimotor cortex, increases the expression of synaptic GluR2 in ipsilateral sensorimotor cortex, which may be mechanisms for CIMT to improve functional recovery after ischemic stroke.
强制性运动疗法（CIMT）已被证明是一种有效的方法，可以在人类和动物研究中恢复中风后的功能缺陷，但它的潜在神经可塑性机制仍不清楚。越来越多的证据表明，中风后的康复与突触可塑性密切相关。因此，我们研究了 CIMT 对中风后大鼠对侧和同侧大脑中突触可塑性的影响。大鼠接受 90 分钟的短暂性大脑中动脉闭塞（MCAO）。CIMT 从中风后 7 天开始，持续两周。中风后 7、14 和 21 天进行改良神经功能缺损评分（mNSS）和阶梯走任务测试。高尔基-考克斯染色用于观察树突和树突棘的可塑性变化。通过 Western blot 检测谷氨酸受体（GluR1、GluR2 和 NR1）的表达。我们的数据表明，急性中风后双侧感觉运动皮层和海马体的树突和树突棘均受到不同程度的损伤。CIMT 治疗增强了同侧和对侧感觉运动皮层中树突和树突棘的可塑性，增加了同侧感觉运动皮层中突触 GluR2 的表达，这可能是 CIMT 改善缺血性中风后功能恢复的机制。
