中文摘要：

目的研究脑梗死大鼠经低频电刺激治疗后，其梗死灶镜区脑皮质突触可塑性变化，初步从分子水平探讨低频电刺激治疗的基本机制。方法将48只Sprague—Dawley大鼠随机分为低频电刺激组、安慰刺激组和假手术组。造模术后3d，低频电刺激组接受低频电刺激治疗7d（20min／d）；安慰刺激组安放电极但不予电刺激；假手术组无特殊处置。以电子显微镜观察各组动物脑梗死灶镜区突触超微结构，采用Westernblot技术测定其胶质纤维酸性蛋白（GFAP）和突触素的蛋白表达水平。结果低频电刺激治疗7d后，与安慰刺激组及低频电刺激治疗前相比，镜区皮质突触的界面曲率增大、突触间隙缩窄；GFAP蛋白表达水平无显著改变，而突触素蛋白表达水平显著升高（P〈0．05）。结论低频电刺激可诱导脑梗死大鼠梗死灶镜区脑皮质发生活跃的突触可塑性变化。

英文摘要：

Objective To study changes in synaptic plasticity in the contralesional mirror area of the cor- texes of rats with cerebral infarction treated by low-frequency electrical stimulation （LFES） and to explore the thera- peutic mechanism of LFES on the molecular level. Methods Forty-eight Sprague-Dawley rats were randomly al- located into a LFES group, a placebo group and a sham-operation group. Following middle cerebral artery occlusion （MCAO）, rats in the LFES group were treated with LFES for 7 d （20 rain/d） , while the ones in placebo group were connected with the same LFES device but without electricity. Rats in the sham-operation group were subjected to a MCAO operation without occlusion and then received no special treatment. Synaptic ultra-structures and the ex- pression levels of gila fibrillary acidic protein （GFAP） and synaptophysin in the contralesional mirror area of the eortexes of the rats in each group were measured with electron-microscopy and Western blotting. Results Com.- pared with the placebo group or the rats before treatment, rats treated with LFES exhibited ultra-structural changes in the form of larger curvature of synaptic interfaces and narrower synaptic clefts. GFAP expression levels did not fluctuate significantly, but the expression of synaptophysin was significantly up-regulated. Conclusion LFES treatment can induce active changes in synaptie plasticity in the eontralesional mirror area of the cortex of rats after cerebral infarction.