P77PMC大鼠惊厥后脑内N—甲基—D—门冬氨酸受体功能的研究

目的 探讨惊厥后大脑皮质N－甲基－D－门冬氨酸（NMDA）受体兴奋性的改变与癫Xian发病机制的关系。方法 利用配基结合实验观察听源性惊厥大鼠P77PMC惊厥前后大脑皮质突触膜对^3H-MK 801的结合改变以及不同激动剂组合对其结合的影响。结果 反应体系中无任何NMDA受活动剂时，惊厥后大脑皮质突触膜对^3H-MK 801的结合有增加趋势，但无统计学意义；当反应液中加入NMDA受体激动剂时，惊厥后大脑皮质突触膜对^3H-MK 801的结合明显增加，除惊厥后4h与正常对照组相比无统计学差异外，其他惊厥后各时间点与正常对比均有统计学差异（P＜0．01）。结论 听源性惊厥大鼠P77PMC惊厥后，大脑皮质NMDA受体活性增高，对其激动剂的敏感性增加，受体通道更易被打开。

The function change of NMDA receptor in P77PMC rat brain after audiogenic seizure

Objective NMDA receptor plays a key role in the initiation and spread of seizure activity and is associated with the epileptogenesis and the synaptic plasticity in the central nervous system. The study was to research the excitability of the receptor after seizure and the pathogenesis of epilepsy.Methods Radio-ligand binding assay was used to detect the functional activity of the NMDA receptor after audiogenic seizure by measuring the binding of 3H-MK 801, the NMDA receptor open-channel blocker, to the P77PMC rat cortex membrane.Results No statistically significant alterations were detected when none of glutamate,glycine or spermine exists in the reactive system, but when the agonists exist in the reactive system, the increased sensitivity of 3H-MK 801 binding to the stimulatory action of glutamate, glycine and spermidine was significant.Conclusion The synaptic activation of NMDA receptor is increased after seizure and the channel is easily opened.