本研究目的为探讨谷氨酸钠(GluNa)诱导大鼠癫痫发作时海马mGluR5的表达变化.将动物随机分为正常对照组、Glu-Na致痫组及D AP-5(非竞争性NMDA受体拮抗剂)+GluNa组.通过免疫组织化学方法观察了多克隆抗体抗mGluR5在海马各区及齿状回的免疫反应阳性细胞的变化,同时观察并记录各组大鼠的行为变化.结果证明:GluNa注射后的大鼠均出现严重的癫痫发作.正常组大鼠海马中有丰富的mGluR5表达,以齿状回颗粒细胞层和CA1锥体细胞层的表达为最高,而GluNa致痫组海马各区mGluR5表达明显下调.D-AP 5+GluNa组海马各区mGluR5表达较之GluNa致痫组又上调.同时观察到三个组的mGluR5的表达主要集中在细胞膜上.结果提示mGluR5在癫痫发作后表达下降可能在癫痫诱导过程中具有重要作用,其作用机制可能为NMDA受体依赖性的.
The altered expression of metabotropic glutamate receptor subtype 5(mGluR 5) in the hippocampus of sodium glutamate kindled rats was investigated. All rats were divided randomly into three groups: control group; sodium glutamate group; and D-AP-5(noncompetitive NMDA receptor antagonist)+GluNa group. Polyclonal antibody specific for mGluR 5 was used to observe the immunoreaction for mGluR 5 in dentate gyrus and the other regions of hippocampus. Behaviour changes of all rats were simultaneously observed. The results showed that all rats of GluNa group exhibited severe convulsion. The expression of mGluR 5 in the rats of control group was very high, especially in the granular layer of dentate gyrus and the pyramidal layer of CA 1. Whereas an initial down regulation of mGluR 5 was observed in all the regions of hippocampus of rats from sodium glutamate group. At the same time the expression of mGluR 5 in the group of D-AP-5+GluNa was increased compared to that of GluNa group. The expression of mGluR 5 was mainly on membrane. The results suggest that the down regulation of mGluR 5 expression after the kindled seizure may play an important role in the procedure of inducing epilepsy. The mechanism of the function of mGluR 5 might be NMDA receptor dependent.
Chinese Journal of Neuroanatomy