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大鼠大脑损伤后皮质NMDA受体活性变化与脑水肿的关系 |
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罗成义 王清华 徐如祥
【摘要】 目的 脑损伤后释放的谷氨酸通过其受体,主要是N-甲基-D-天门冬氨酸(NMDA)受体而发挥神经元兴奋毒作用;通过对脑损伤后不同时期伤侧大脑皮质NMDA受体活性和含水量的测定,探讨它们之间的关系。方法 以自由落体致伤方法制作脑损伤模型,采用放射性配基结合分析法对伤后不同时间的大鼠伤侧大脑皮质NMDA受体进行测定,用干湿法测脑皮质含水量。结果 伤后30分钟脑皮质含水量开始增加,伤后6小时达高峰,伤后168小时恢复正常;NMDA受体的最大结合量(Bmax)于伤后15分钟开始升高,伤后30分钟达高峰,之后逐渐降低,于伤后6小时达最低值,以后逐步升高,伤后72小时基本恢复正常。结论 实验结果提示NMDA受体过度激活是脑损伤后早期继发性脑水肿的重要启动因素之一。
【关键词】 NMDA受体 脑损伤 脑水肿 大鼠
Relationship Between Changes of N-methyl-D-aspartate Receptor Activity on Cerebral Cortex and Brain Edema After Brain Injury in Rats LUO Cheng-yi, WANG Qing-hua, XU Ru-xiang. Dept. of Neurosurgery, Zhujiang Hospital, First Military Medical University, Guangzhou 510282
【Abstract】 Aim To investigate the relationship between the changes of N-methyl-D-aspartate (NMDA) receptor activity on cerebral cortex and brain edema after brain injury in the rats.Methods The brain injury model was made by a free-falling body. Water contents in brain cortex were measured with drying-wet method, and NMDA receptor activity was detected with a radio ligand binding assay.Results The water contents began to increase at 30 minutes and reached peak at 6 hours after brain injury. The maximal binding (Bmax) of NMDA receptor increased significantly at 15 minutes and reached peak at 30 minutes after brain injury, then decreased gradually and had the lowest value at 6 hours after brain injury.Conclusion It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the successive cerebral impairments after brain injury.
【Key words】 N-methyl-D-aspartate receptor Brain injury Brain edema Rat
已有实验表明脑损伤后早期谷氨酸大量释放产生兴奋毒作用,加重脑损伤后继发性损害［1］,但对其如何通过受体产生兴奋毒作用的机制尚不十分明了。谷氨酸受体分为五类即:(1)NMDA受体;(2)海人藻酸(KA)受体;(3)使君子酸盐(QA)受体;(4)L-2-氨基-4-磷丁酸(L-AP4)受体;(5)亲代谢型受体。脑损伤后谷氨酸主要通过NMDA受体发挥继发性损害作用［2］。为此,笔者对脑损伤后不同时期伤侧大脑皮质NMDA受体活性和含水量进行测定,以探讨它们之间关系。
材料与方法
1.主要试剂:［3H］-L-谷氨酸(［3H］-L-Glu,49Ci/mmol, Sigma), CPP(Sigma),玻璃纤维滤纸(海[1] [2] 下一页
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