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目的 探明迷走神经刺激 (VNS)疗法抗癫痫的分子机制 ,为临床工作奠定基础 .方法 利用免疫组化的方法 ,观察 VNS前后 ,红藻氨酸 (KA)致痫大鼠海马及孤束核等相关脑区 Nd酶活性的变化 ,并结合动物行为及脑电图指征探讨一氧化氮 (NO)介质途径在其中的可能作用 .结果 VNS可显著延长 KA诱发的首次全身强直 -阵挛发作 (GTCs)的潜伏期 ,且发作持续时间缩短 ,频率降低 .脑电图异常程度明显减低 .VNS后内侧孤束核及齿状回门区内 Nd阳性细胞数增多 (P<0 .0 1 ) .结论 VNS可有效抑制大鼠 KA诱导性癫痫发作 ,关键脑区内 NO介质生成的阶段性增多可能在其中发挥重要作用
Objective To explore the molecular mechanism of anti-epilepsy induced by vagus nerve stimulation (VNS) and lay the foundation for clinical practice.Methods Immunohistochemical method was used to observe the changes of hippocampus and solitary tract nucleus in kainic acid-induced (KA) rats before and after VNS Related neuropeptide kinase activity in brain and explore the possible role of nitric oxide (NO) pathway in animal behavior and electroencephalogram (EEG) .Results VNS can significantly prolong the first tonic-clonogenic seizure induced by KA GTCs), and the duration of attack was shortened and the frequency was decreased.The abnormality of EEG was significantly reduced.The number of Nd positive cells in medial solitary tract nucleus and dentate gyrus returned after VNS (P <0.01) Conclusion VNS can effectively inhibit KA-induced seizures in rats, and the staged increase of NO mediators in key brain regions may play an important role