摘要
Ｎ－甲基－Ｄ－天门冬氨酸（ＮＭＤＡ）受体与癫痫的产生密切相关，我们以［３Ｈ］ＭＫ－８０１在ＮＭＤＡ受体激动剂作用下与突触膜结合情况，检测了遗传性癫痫易感大鼠Ｐ７７ＰＭＣ的ＮＭＤＡ受体功能。结果显示：１０－６ｍｏｌ·Ｌ－１谷氨酸或１０－６ｍｏｌ·Ｌ－１谷氨酸加１０－６ｍｏｌ·Ｌ－１甘氨酸可促进Ｐ７７ＰＭＣ大鼠大脑皮层、海马对［３Ｈ］ＭＫ－８０１的结合，并显著高于对照。一些抗癌药及生物制剂可降低或促进［３Ｈ］ＭＫ－８０１的结合。提示ＮＭＤＡ受体活性增高是遗传性癫痫易感大鼠惊厥产生的重要因素，以及抗病药的可能作用途径。
The functional acitivity of N-methyl-D-asprtate(NMDA)-sensitive glutamate receptor was examined in cerebral cortex and hippcampus of genetically epilepsy-prone rat(P77PMC).The results showed:(1) 10-6mol·L-1 glutamate or 10-6mol·L-1 glutamate and 10-6 mol·L-1 glycine stimulated a significantly increase of[3H] MK-801 binding in synaptic membranes of cerebral cortex and hippocampus in P77PMC rats.(2) The phenobarbital,carbamazepine and nifedipine were effective in significantly inhibiting binding.The interlugine-1 enhanced increase of [3H] MK-801 binding,which blocked by interlukine-1 receptor antagonist.The results suggest that increase in NMDA receptor activity may contribute to epilepsy susceptibility of P77PMCrats.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1996年第4期313-316,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金
关键词
NMDA
受体
遗传性
癫痫
谷氨酸
甘氨酸
NMDA receptor
[￣3H] MK-801binding
genetically epilepsy-prone rat
glutamate
glycine
