经颅磁刺激治疗对脑梗死大鼠健侧感觉运动皮质锥体细胞树突和突触结构的影响

目的观察经颅磁刺激(TMS)对大鼠局灶脑梗死后神经功能恢复和健侧皮质树突、突触结构的影响,探讨其作用机理。方法 24只雄性 SD 大鼠应用线栓法建立大鼠局灶脑梗死模型,随机分为 TMS 组和自然恢复组,前者给予 TMS 治疗28 d,后者常规饲养,观察大鼠神经功能恢复情况和健侧大脑感觉运动皮质锥体细胞树突和突触结构参数的变化。结果 TMS 组大鼠 Bederson 神经功能缺损评分(0.58±0.49)明显低于自然恢复组(0.92±0.28)(P<0.05);TMS 组运动皮质锥体细胞树突总长度(898±127)μm、一级树突分支数(6.6±1.5)个和单位长度树突棘密度(0.75±0.19)个/μm均明显高于自然恢复组(788±112)μm、(5.8±1.5)个、(0.60±0.16)个/μm(P<0.05或0.01);突触界面曲度(1.06±0.08)明显大于自然恢复组(1.02±0.06)(P<0.05),突触后致密物质(PSD)厚度(64±13)nm 较自然恢复组(54±12)nm 明显增厚(P<0.01),突触间隙(19.5±2.1)nm明显窄于自然恢复组(23.3±2.3)nm(P<0.0I)。结论 TMS 可促进脑缺血大鼠神经功能的改善,其机制可能与健侧感觉运动皮质锥体细胞树突和突触结构参数的改变有关。

Effects of transcranial magnetic stimulation on recovery of neural functions and changes of synaptic interface and dendritic structure in the contralateral brain area after cerebral infarction: experiment with rats

OBJECTIVE: To evaluate the effects of transcranial magnetic stimulation (TMS) on the brain plasticity and its role in functional outcome in cerebral infarction. METHODS: Twenty male SD rats underwent suture of the unilateral middle cerebral artery (MCA) so as to establish focal cerebral infarction models and then were randomly divided into 2 equal groups: model group, to be reared in the original living state, and TMS group, given in addition TMS treatment 1 day after infarction 2 times per day and 30 pulses per time for 4 weeks. Twenty-eight days after the rats were killed. Four rats from each group underwent microscopy of the brain to measure the dendritic structure of the pyramidal cells quantitatively. Other 4 rats from each group underwent electron microscopy of the brain to measure the parameters of synaptic interface in the sensorimotor cortex. Neural function scoring was conducted 24 hours after the establishment of model and before being killed. RESULTS: There was no significant difference in the neural function 24 h after the establishment of models, however, 28 days after the score of neural function of the TMA group was 0.58 +/- 0.49, significantly lower than that of the model group (0.92 +/- 0.28, P < 0.05). The total dendritic length, number of dendritic branching points, and dendritic density in layer V pyramidal cells within the undamaged motor cortex of the TMS group were 898 microm +/- 127 microm, 6.6 +/- 1.5, and 0.75/microm +/- 0.19/microm, all significantly higher than those of the model group (788 microm +/- 112 microm, 5.8 +/- 1.5, and 0.60/microm +/- 0.16/microm, P < 0.05 or < 0.01). Electron microscopy showed that the synaptic curvatures and post-synaptic density of the TMS group were 1.06 +/- 0.08 and 64 +/- 13 respectively, both significantly higher than those of the model group (1.02 +/- 0.06 and 54 +/- 12 nm respectively, P < 0.05 and P < 0.01), and the synapse cleft width of the TMS group was 19.5 +/- 2.1, significantly narrower than that of the model group (23.3 +/- 2.3, P < 0.01). CONCLUSION: TMS promotes the improvement of neural functions of the rats with cerebral ischemia by the potential mechanism that TMS strengthen the compensatory roles of the synaptic interface and dendritic structure in the undamaged sensorimotor cortex area and increase synaptic plasticity.