重复经颅磁刺激（rTMS）是缺血性卒中（IS）后运动功能残疾的重要康复手段。研究表明IS后胶质瘢痕可分泌硫酸软骨素蛋白多糖（CSPGs）阻碍轴突生长，影响运动功能康复，但rTMS是否通过调控胶质瘢痕的形成促进IS后运动康复尚不清楚。我们预实验发现高频rTMS减少IS后胶质瘢痕的形成，下调CSPGs的表达，同时导致TGFβ-Smad2/3信号通路的激活减少；且星形胶质细胞内参与Smad2/3激活的KCa3.1通道表达下降。但rTMS是否通过KCa3.1通道抑制胶质瘢痕形成而改善IS后的运动功能及具体机制尚不清楚。本项目拟通过体内外实验证明：rTMS通过下调IS后星形胶质细胞KCa3.1通道，抑制TGFβ-Smad2/3通路的激活，从而减少胶质瘢痕的过度形成及CSPGs分泌，促进神经元轴突生长。本项目将阐明rTMS治疗IS后运动残疾的新机制，并为增强rTMS对IS的康复疗效提供可能的药物靶点。

Repetitive transcranial magnetic stimulation (rTMS) is an important treatment for motor function disability after ischemic stroke (IS). Studies have shown that glial scars can secrete chondroitin sulfate proteoglycans (CSPGs) to hinder axon growth and affect motor function recovery, but whether rTMS improve the motor function disability after IS through reducing the formation of glial scars is still unknown. Our preliminary experiments found that high-frequency rTMS reduces the formation of glial scars after IS, down-regulates the expression of CSPGs, and leads to a deactivation of TGFβ-Smad2/3 signaling pathway; and meanwhile the expression of KCa3.1 channel which involved in Smad2/3 activation in astrocyte decreases. However, whether rTMS inhibits the formation of glial scars via the KCa3.1 channel and thus improves the motor function in IS and the specific mechanism are not clear. This project intends to verify the following hypothesis via in vivo and in vitro experiments：rTMS inhibits the activation of TGFβ-Smad2/3 pathway by down-regulating KCa3.1 Channel in astrocytes, then reducing the excessive formation of glial scars and the secretion of CSPGs, thereby promoting the growth of neuronal axons . This project will clarify the new mechanism for treatment of motor function disabilities by rtTMS in IS, and provide a possible drug target for enhancing the rehabilitation effect of rTMS on IS.