经颅磁刺激对短暂性大脑中动脉闭塞大鼠突触素表达和超微结构改变的影响

Effect of Transcranial Magnetic Stimulation on Synaptophysin Expression and Ultrastructural Changes After Transient Middle Cerebral Artery Occlusion in Rats

目的:研究经颅磁刺激(TMS)对短暂性大脑中动脉闭塞(MCAO)大鼠突触素表达和超微结构改变的影响。方法:TMS组与假刺激组成年大鼠各32只,于MCAO/再灌注(MCAO/R)120min后3周内接受TMS与假刺激处理。在处理不同时间段检测梗死灶周围突触素(SY38)免疫阳性产物表达,透射电镜下观察刺激21d后缺血侧脑皮质缺血半暗带血管、神经细胞和突触变化。另设正常组6只,假手术组6只,检测脑内SY38免疫阳性产物表达。结果:在刺激1d和3d后,两组SY38免疫阳性物质表达均持续降低,刺激7d后逐渐恢复升高。与假刺激组各对应点相比,TMS组在刺激7d、14d和21d后梗死灶周围SY38免疫阳性物质表达显著增高(P<0.05)。透射电子显微镜观察提示,刺激21d后TMS组的神经元整体细胞超微结构缺血性损伤好于假刺激组,线粒体肿胀程度较轻,血管周围结构紧密完整,突触界面曲率相对更大,突触间隙变窄,突触后致密物质增厚。结论:长程TMS可以上调脑梗死周围区SY38的表达,减轻缺血周围区毛细血管和神经组织损伤,促进突触超微结构的重建和功能增强,提示TMS有助于促进缺血脑损伤的恢复,促进脑组织神经网络重建和脑可塑性增加是其可能的机制之一。

Objective： To investigate the effect of transcranial magnetic stimulation （rIMS） on synaptophysin expression and cortical ultrastructural changes after transient middle cerebral artery occlusion （MCAO） in rats. Methods： Adult SD rats were divided into a rIMS group and a sham rIMS group （n = 32 in each group）, and they received rIMS and sham rIMS within 3 weeks after MCAO/reperfusion （MCAO/R） for 120 min. The expressions of synaptophysin （SY38） immunopositive products around the infarcted areas were detected in the different periods after rIMS. The changes of blood vessels, neural cells, synapse in the affected cortical ischemic penumbra were observed by transmission electron microscope 21 days after rIMS. A normal group and a sham group （n =6 in each） were also set up, and the expressions of SY38 immunopositive products in brain were detected. Results： The expressions of SY38 immunopositive products in both groups decreased continuously 1 and 3 days after rIMS, and they increased gradually 7 days after rIMS. As compared with the sham rIMS group, the expressions of SY38 immunopositive products around the infarcted areas after 7-, 14-, and 21 -day stimulation in the rIMS group increased significantly （P 〈0.05）. The observation of transmission electron microscope showed that the ischemic injury of the ultrastructures in neuronal whole-cell after 21-day stimulation in the rIMS group was better than that in the sham rIMS group, and the mitochondria swelling was slighter, the ultrastructures around blood vessels were tight and integrated, the curvature of the synaptic interface was relatively larger, the synaptic cleft became narrow, and the postsynaptic densities thickened. Conclusions： The long-term TMS may upregulate the expressions of SY38 around the areas of cerebral infarction, lessen capillary vessels and nerve tissue injuries in the peripheral areas of ischemia, promote the reconstruction and functional enhancement of synaptic ultrastructures. It is suggested that TMS contribute to promote the recovery of cerebral ischemic injury. Facilitating the reconstruction of neural network and increasing brain plasticity are one of its possible mechanisms.