摘要
目的 探讨迷走神经刺激 (vagus nerve stimulation,VNS)抗癫痫的机制。方法 应用原位杂交组织化学方法研究戊四氮 (PTZ)致癫痫大鼠和 VNS抗癫痫大鼠丘脑网状核谷氨酸受体 (NMDAR1 ) m RNA的变化。结果 丘脑网状核 NMDAR1 m RNA表达 ,PTZ致癫痫组明显高于正常对照组 ,VNS抗癫痫组明显低于 PTZ致癫痫组 ,VNS抗癫痫组与正常对照组之间差异无显著性。结论 (1 )丘脑网状核在 PTZ致癫痫和 VNS抗癫痫中均可能起着重要作用。 (2 ) VNS可能通过抑制丘脑网状核兴奋性神经递质受体—— NMDAR的活性与表达 ,降低大脑皮层的兴奋性 ,从而提高癫痫发作的阈值 ,抑制癫痫的形成及发展来发挥抗癫痫作用。
Objective To explore the possible antiepileptic mechanism of vagus nerve stimulation (VNS).Methods The expression of NMDAR1 mRNA in the thalamic reticular nuclei was determined by in situ hybridization and image analysis.Results The expression of NMDAR1 mRNA in thalamic reticular nuclei of PTZ group rats was higher than that of control group rats. After treatment with VNS, the expression decreased.Conclusions (1)The thalamic reticular nuclei may play an important role in the pentylenetetrazole induced epileptogenesis and in the antiepileptic effect of VNS.(2)VNS may suppress the activities and expression of NMDAR in thalamic reticular nuclei, and reduce the excitability of cerebral cortices.The development and episode of epilepsy were inhibited, by raising the threshold of seizure.
出处
《中国神经免疫学和神经病学杂志》
CAS
2002年第3期125-127,F003,共4页
Chinese Journal of Neuroimmunology and Neurology
