Constraint-induced movement therapy improves functional recovery after ischemic stroke and its impacts on synaptic plasticity in sensorimotor cortex and hippocampus

• Published in: Brain research bulletin Vol. 160; pp. 8 - 23
• Main Authors: Hu, Jian, Li, Ce, Hua, Yan, Liu, Peile, Gao, Beiyao, Wang, Yuyuan, Bai, Yulong
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.07.2020
• Subjects: Constraint-induced movement therapy; Dendrite; Dendritic spine; Glutamate receptor; Stroke; Synaptic plasticity; Dendritic spine; Stroke; Glutamate receptor; Constraint-induced movement therapy; Synaptic plasticity; Dendrite
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/j.brainresbull.2020.04.006

•CIMT improved functional recovery in rats after ischemic stroke.•CIMT enhanced dendritic complexity in ipsilateral sensorimotor cortex following stroke.•CIMT increased dendritic spines density and functional spines in contralateral sensorimotor cortex following stroke.•CIMT increased synaptic GluR2 expression in ipsilateral sensorimotor cortex following stroke. 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.