Structural plasticity of motor cortices assessed by voxel-based morphometry and immunohistochemical analysis following internal capsular infarcts in macaque monkeys.

Cerebral cortex communications Pub Date : 2022-11-08 eCollection Date: 2022-01-01 DOI:10.1093/texcom/tgac046
Kohei Matsuda, Kazuaki Nagasaka, Junpei Kato, Ichiro Takashima, Noriyuki Higo
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Abstract

Compensatory plastic changes in the remaining intact brain regions are supposedly involved in functional recovery following stroke. Previously, a compensatory increase in cortical activation occurred in the ventral premotor cortex (PMv), which contributed to the recovery of dexterous hand movement in a macaque model of unilateral internal capsular infarcts. Herein, we investigated the structural plastic changes underlying functional changes together with voxel-based morphometry (VBM) analysis of magnetic resonance imaging data and immunohistochemical analysis using SMI-32 antibody in a macaque model. Unilateral internal capsular infarcts were pharmacologically induced in 5 macaques, and another 5 macaques were used as intact controls for immunohistochemical analysis. Three months post infarcts, we observed significant increases in the gray matter volume (GMV) and the dendritic arborization of layer V pyramidal neurons in the contralesional rostral PMv (F5) as well as the primary motor cortex (M1). The histological analysis revealed shrinkage of neuronal soma and dendrites in the ipsilesional M1 and several premotor cortices, despite not always detecting GMV reduction by VBM analysis. In conclusion, compensatory structural changes occur in the contralesional F5 and M1 during motor recovery following internal capsular infarcts, and the dendritic growth of pyramidal neurons is partially correlated with GMV increase.

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猕猴内包膜梗死后运动皮质结构可塑性的体素形态学和免疫组织化学分析。
在剩余的完整大脑区域的代偿性可塑性变化被认为与中风后的功能恢复有关。在此之前,大脑皮层激活的代偿性增加发生在腹侧运动前皮层(PMv),这有助于猕猴单侧内包膜梗死模型灵巧手运动的恢复。在此,我们利用基于体素的形态学分析(VBM)对猕猴模型的磁共振成像数据进行分析,并使用SMI-32抗体进行免疫组织化学分析,研究了功能变化背后的结构塑性变化。用药物诱导5只猕猴单侧内包膜梗死,另取5只猕猴作为完整对照,进行免疫组化分析。梗死后3个月,我们观察到对侧吻侧PMv (F5)和初级运动皮层(M1)的灰质体积(GMV)和V层锥体神经元的树突树突化显著增加。组织学分析显示,尽管VBM分析并不总能检测到GMV的减少,但同病M1和几个运动前皮层的神经元体和树突萎缩。综上所述,内包膜梗死后运动恢复过程中,对侧F5和M1发生代偿性结构变化,锥体神经元树突生长与GMV增加部分相关。
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