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脑源性神经营养因子-TrkB 通路在缺血性脑卒中大鼠突触可塑性中的作用。

Brain-Derived Neurotrophic Factor-TrkB Pathway on Synaptic Plasticity in Ischemic Stroke Rats.

机构信息

Department of Laboratory Animals, College of Animal Sciences, Jilin University.

出版信息

Int Heart J. 2024;65(6):1095-1106. doi: 10.1536/ihj.24-312.

Abstract

Stroke poses a serious risk to human health. The incidence of stroke is increasing year by year. In this study, a rat cerebral ischemiareperfusion (middle cerebral artery occlusion) model was established, and the reliability of this model was determined.The expression changes of key proteins of the BDNF TrkB pathway and synaptic plasticity markers (SYP, PSD-95, and MAP-2) were detected at different time points.The results showed that BDNF expression increased rapidly in the acute phase, and the expression of synaptic plasticity markers decreased, and blocking the BDNF-TrkB pathway with the specific blocker K252a also had a significant effect.This suggests that changes in the BDNF-TrkB signaling pathway can affect the synaptic plasticity in nerve cells of stroke patients.

摘要

中风对人类健康构成严重威胁。中风的发病率逐年上升。在本研究中,建立了大鼠脑缺血再灌注(大脑中动脉闭塞)模型,并确定了该模型的可靠性。检测了 BDNF-TrkB 通路关键蛋白和突触可塑性标志物(SYP、PSD-95 和 MAP-2)在不同时间点的表达变化。结果表明,BDNF 在急性期迅速增加,突触可塑性标志物表达减少,而用特异性阻滞剂 K252a 阻断 BDNF-TrkB 通路也有显著效果。这表明 BDNF-TrkB 信号通路的变化会影响中风患者神经细胞的突触可塑性。

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