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tDCS Accelerates the Rehabilitation of MCAO-Induced Motor Function Deficits via Neurogenesis Modulated by the Notch1 Signaling Pathway
Neurorehabilitation and Neural Repair ( IF 4.2 ) Pub Date : 2020-06-16 , DOI: 10.1177/1545968320925474
Keying Zhang 1, 2 , Ling Guo 1, 2 , Junping Zhang 1, 2 , Gang Rui 1, 2 , Guangzhou An 1, 2 , Yan Zhou 1, 2 , Jiajin Lin 1, 2 , Junling Xing 1, 2 , Tao Zhao 1, 2 , Guirong Ding 1, 2
Affiliation  

Background. Ischemic stroke carries a high mortality rate and is a leading cause of severe neurological disability. However, the efficacy of current therapeutic options remains limited. Objective. We aimed to investigate the treatment efficacy of transcranial direct current stimulation (tDCS) in motor function rehabilitation after ischemic stroke and explore the underlying mechanisms. Methods. Male Sprague-Dawley rats with epicranial electrodes were used to establish pathogenetic model through temporary right middle cerebral artery occlusion (MCAO). Subsequently, animals were randomly divided into 4 groups: MCAO + tDCS/sham tDCS, Control + tDCS/sham tDCS. Animals in the groups with tDCS underwent 10 days of cathodal tDCS totally (500 µA, 15 minutes, once a day). During and after tDCS treatment, the motor functions of the animals, ischemic damage area, proliferation and differentiation of neural stem cells (NSCs), and distribution, and protein expression of Notch1 signaling molecules were detected. Results. The rehabilitation of MCAO-induced motor function deficits was dramatically accelerated by tDCS treatment. NSC proliferation in the subventricular zone (SVZ) was significantly increased after MCAO surgery, and tDCS treatment promoted this process. Additionally, NSCs probably migrated from the SVZ to the ischemic striatum and then differentiated into neurons and oligodendrocytes after MCAO surgery, both of which processes were accelerated by tDCS treatment. Finally, tDCS treatment inhibited the activation of Notch1 signaling in NSCs in the ischemic striatum, which may be involved in NSC differentiation in the MCAO model. Conclusion. Our results suggest that tDCS may exert therapeutic efficacy after ischemic stroke in a regenerative medical perspective.

中文翻译:

tDCS 通过 Notch1 信号通路调节的神经发生加速 MCAO 诱导的运动功能缺陷的康复

背景。缺血性中风的死亡率很高,是导致严重神经功能障碍的主要原因。然而,当前治疗选择的功效仍然有限。目标。我们旨在研究经颅直流电刺激 (tDCS) 在缺血性脑卒中后运动功能康复中的治疗效果并探讨其潜在机制。方法。使用带有颅外电极的雄性 Sprague-Dawley 大鼠通过暂时性右侧大脑中动脉闭塞(MCAO)建立发病模型。随后,将动物随机分为 4 组:MCAO + tDCS/sham tDCS,Control + tDCS/sham tDCS。tDCS 组中的动物总共接受了 10 天的阴极 tDCS(500 µA,15 分钟,每天一次)。在 tDCS 治疗期间和之后,动物的运动功能,检测缺血损伤面积、神经干细胞(NSCs)的增殖和分化,以及 Notch1 信号分子的分布和蛋白表达。结果。tDCS 治疗显着加速了 MCAO 引起的运动功能缺陷的康复。MCAO 手术后脑室下区 (SVZ) 的 NSC 增殖显着增加,tDCS 治疗促进了这一过程。此外,在 MCAO 手术后,NSCs 可能从 SVZ 迁移到缺血性纹状体,然后分化为神经元和少突胶质细胞,这两个过程都被 tDCS 治疗加速。最后,tDCS 治疗抑制了缺血性纹状体中 NSC 中 Notch1 信号的激活,这可能与 MCAO 模型中的 NSC 分化有关。结论。
更新日期:2020-06-16
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