听原性惊厥易感大鼠下丘GluR2的表达及QR位点编辑水平

听原性惊厥易感大鼠是强直 -阵挛惊厥大发作的一种模型 .一般认为 ,下丘是听原性惊厥发作神经元网络的启动部位 .采用RT PCR、Western印迹、免疫组织化学等方法观察了听原性惊厥易感大鼠 (P77PMC)一次惊厥发作与惊厥点燃状态下AMPA受体亚基GluR2在下丘内表达的改变 ,并采用限制性酶切方法分析了GluR2Q R位点mRNA编辑水平的改变 .研究结果显示 ,一次惊厥发作后下丘内GluR2表达无明显改变 ,惊厥点燃后下丘内GluR2表达降低 ,一次惊厥发作及惊厥点燃状态下GluR2Q R位点处于编辑成熟状态 .提示 ,GluR2表达降低参与了点燃状态下的惊厥发作 ,在听原性惊厥易感大鼠惊厥发作机制中不涉及下丘内GluR2Q R位点编辑水平改变 .

Expression and Editing Status of Glutamate Receptor GluR2 Subunit in Audiogenic Seizure Susceptible P77PMC Rats

The audiogenic seizure (AGS) susceptible rat is a model of generalized tonic clonic epilepsy. The inferior colliculus (IC) is established as the initiation site within the neuronal network for audiogenic seizures. Using RT-PCR, Western blot and immunocytochemistry methods, the expression of GluR2 was examined after single AGS and AGS kindling in the IC of P77PMC rat. The levels of mRNA editing of GluR2 at Q/R site were observed by restriction enzyme digest. Consequently, single AGS had no effect on the expression of GluR2 in the IC of P77PMC rat, though repetition audiogenic seizure (kindling) resulted in the decreases of GluR2 in the IC. Only complete edited form of the GluR2 at the Q/R site could be detected in single AGS and kindling. These results suggest that the decreases of the GluR2 subunit may play a role in the mechanism of AGS kindling. Alteration of the editing process of GluR2 may not be involved in AGS.