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目的研究经颅磁刺激(TMS)对脑梗死后大鼠学习记忆功能,以及海马锥体细胞树突和突触结构的影响。方法将48只雄性SD大鼠随机分为正常组、模型组和TMS组,每组16只。采用线栓法对模型组和TMS组大鼠制作一侧大脑中动脉闭塞的脑梗死模型,并在制模后第2天,对TMS组给予每天2次、每次30个脉冲的TMS治疗,疗程4周;观察各组大鼠治疗后在Y-迷宫中的学习记忆成绩和梗死对侧海马锥体细胞树突和突触结构变化。结果(1)TMS组大鼠学习尝试次数[(18.4±4.8)次]少于模型组[(26.4±5.4)次;P<0.01],记忆再现次数[(6.1±1.3)次]多于模型组[(3.7±1.2)次;P<0.01];(2)TMS组海马CA3区锥体细胞树突顶树突总长度[(196±35)μm]长于模型组(175±33)μm;P<0.01]。(3)TMS组的突触后致密物质厚度[(68±11)nm]宽于模型组[(62±10)nm],穿孔性突触百分比(27.5%)高于模型组(10.0%),突触间隙[(16.7±1.8)nm]窄于模型组[(21.3±2.3)nm],均P<0.01和P<0.05。结论TMS能促进脑梗死大鼠学习记忆功能的恢复,其机制可能与海马锥体细胞树突和突触结构的改变有关。
Objective To study the effects of transcranial magnetic stimulation (TMS) on learning and memory and the dendrites and synapses of pyramidal cells in rats after cerebral infarction. Methods 48 male SD rats were randomly divided into normal group, model group and TMS group, with 16 rats in each group. A cerebral infarction model of middle cerebral artery occlusion (MCAO) was made in the model group and the TMS group by the method of thread embolism. TMS group was given twice-daily TMS treatment of 30 pulses on the second day after model establishment. The courses of learning and memory in the Y-maze and the changes of dendrites and synapses in the contralateral hippocampal pyramidal cells were observed. Results (1) The number of learning attempts in TMS group was (18.4 ± 4.8) times less than that in model group (26.4 ± 5.4), P <0.01, and the number of memory replays was (6.1 ± 1.3) Group [(3.7 ± 1.2) times; P <0.01]; (2) The total length of dendritic dendrites in hippocampal CA3 pyramidal neurons in TMS group was (196 ± 35) μm longer than that in model group (175 ± 33) μm; P <0.01]. (3) The thickness of postsynaptic density in TMS group (68 ± 11) nm was significantly higher than that in model group (62 ± 10 nm), and the percentage of perforation synapse (27.5%) was higher than that in model group (10.0% , And the synaptic clearance [(16.7 ± 1.8) nm] was narrower than that in the model group [(21.3 ± 2.3) nm], both P <0.01 and P <0.05. Conclusion TMS can promote the recovery of learning and memory in rats with cerebral infarction. Its mechanism may be related to the changes of dendrites and synapses in pyramidal cells of hippocampus.