摘要
目的 :探讨迷走神经刺激 (VNS)抗癫作用的细胞机制。 方法 :用戊四氮 (PTZ)行大鼠腹腔注射点燃制作癫模型 ,行迷走神经刺激抗癫 ,应用荧光分光光度法测定不同浓度谷氨酸 (Glu)对正常、PTZ点燃及 VNS治疗动物大脑皮质及海马神经元胞内游离钙升高的影响 ,同时观察 VNS对动物癫行为的影响。 结果 :VNS组动物胞内游离钙浓度较 PTZ点燃组明显降低 ,并对外源性 Glu的升高胞内游离钙有明显抑制作用 ,行为观察显示VNS能明显抑制癫发作的严重程度 ,延长癫发作的潜伏期。 结论 :VNS能明显抑制大鼠 PTZ的点燃效应 ,降低 Glu对神经元胞内游离钙的升高作用。 VNS可能通过调节神经元兴奋性
Objectives:To explore the antiepileptic cellular mechanism of chronic vagus nerve stimulation (VNS). Methods: The rats were kindled by intraperitoneal injection of pentylenetetrazol (PTZ) (45mg/kg weight), and chronic VNS was applied to the kindled rats. The effects of glutamate (Glu) on the intracellular free calcium ([Ca 2+ ]i) of cortical and hippocampal neurons of normal, PTZ kindled and VNS treated rats were examined with fluorescence spectrophotometry respectively. The behavioral changes of all rats were observed. Results: The neuronal [Ca 2+ ]i of the VNS treated rats were significantly lower than that of the PTZ kindled rats. VNS could significantly inhibit the augmentation of neuronal [Ca 2+ ]i induced by Glu. Behavioral changes demonstrated that VNS could significantly reduce the severity and prolong the latency of seizures of PTZ kindled rats. Conclusions: VNS could significantly inhibit the kindling effect of PTZ and reduce the excitability of neurons induced by Glu. VNS might exerted the antiepileptic effects by influencing the activation of neural receptors.
出处
《医学研究生学报》
CAS
2001年第3期207-209,,212,,共4页
Journal of Medical Postgraduates
关键词
迷走神经刺激
癫痫
点燃
谷氨酸
胞内游离钙
Vagus nerve stimulation
Seizure
Kindling
Glutamate
Intracellular free calcium
