迷走神经刺激影响致痫大鼠丘脑神经递质受体活动的实验研究  

The study of activities of neurotransmitter of thalami by vagus nerve stimulation in epileptic rats

作　　者：张晓琴[1] 徐艳[1] 张锦华[1] 

机构地区：[1]武汉大学中南医院神经科,430071

出　　处：《卒中与神经疾病》2003年第1期30-32,共3页Stroke and Nervous Diseases

摘　　要：目的　探讨迷走神经刺激 (VagusNerveStimulation ,VNS)抗癫痫的机制。 方法　应用原位杂交组织化学及图像分析方法研究了戊四氮 (pentylenetetrazol,PTZ)致痫大鼠丘脑网状核γ 氨基丁酸A受体(GABAAR)α1亚单位mRNA的变化。结果　PTZ致痫组大鼠丘脑网状核GABAARα1mRNA表达明显低于正常对照组 ,而VNS抗癫痫组明显高于PTZ致癫痫组。结论　VNS可能通过增强抑制性神经递质受体α 氨基丁酸受体的活动 ,降低大脑皮层的兴奋性 ,从而抑制癫痫的形成及发展。Objective To study the antiepileptic mechanism of vagus nerve stimulation (VNS). Methods We used the methods of in situ hybridyzation and image analysis to detect the expression of GABA A receptor alphal subunit mRNA (GABA ARα1 mRNA) in the thalamic reticular nuclei. Results The expression of GABA ARα1 mRNA in the thalamic reticular nuclei of PTZ group rats was lower than that of control group rats. For rats treated with VNS beforehand, the expression increased. Conclusions VNS may reduce the excitability of cerebral cortices by promoting the activities of gamma aminobutyric acid receptor (GABAR) in thalamic reticular nuclei. So the formation and development of seizures are inhibited.

关 键 词：大鼠 丘脑 神经递质 实验研究 癫痫 迷走神经 Γ-氨基丁酸受体 

分 类 号：R742.1[医药卫生—神经病学与精神病学]