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目的 观察电磁脉冲 (EMP)辐射对大鼠海马组织中N 甲基 D 天门冬氨酸 (NMDA)受体的影响 ,以深入探讨EMP致学习记忆障碍的机制。方法 EMP辐射条件为 6× 10 4V/m ,脉冲上升时间 2 0ns ,脉宽 3 0 μs ,频率 2 .5脉冲 /min ,作用 2min。二级雄性Wistar大鼠 3 2只 ,随机分为EMP组 (n =2 6)和对照组(n =6)。EMP组大鼠分别于辐射后即刻 ,3h ,6h ,2 4h和 48h断头取脑 ,剥离海马 ,制备膜受体蛋白 ,以3 H Glu为配基进行放射性配基 受体结合实验。结果 EMP辐射后即刻大鼠海马中NMDA受体的Kd值开始下降 ,辐射后 3h下降最显著 (与对照组相比 ,P <0 .0 5 ) ,6h渐有恢复 ,48h恢复至正常水平 ;受辐射的大鼠海马中NMDA受体的Bmax值于辐射后 3h和 6h显著下降 (与对照组相比 ,均P <0 .0 5 ) ,2 4h渐有恢复 ,辐射后 48hBmax值明显升高 ,超过对照组水平 (P <0 .0 5 )。结论 EMP辐射可引起大鼠海马组织中NMDA受体亲和力升高及受体密度下降。提示NMDA受体密度、亲和力的改变以及NMDA Ca2 + NO路径的兴奋毒性作用可能参与了EMP致实验动物认知障碍的分子机制。
Objective To observe the effect of electromagnetic pulse (EMP) radiation on N-methyl D-aspartate (NMDA) receptor in hippocampus of rats to investigate the mechanism of EMP-induced learning and memory impairment. Method EMP radiation conditions of 6 × 10 4V / m, pulse rise time 20ns, pulse width 30μs, frequency of 2.5 pulses / min, the role of 2min. Three 2 male Wistar rats were randomly divided into EMP group (n = 26) and control group (n = 6). Rats in EMP group were sacrificed at 3h, 6h, 24h and 48h after radiation. The hippocampus was dissected and the membrane receptor protein was prepared. Radioactive ligand binding experiments were performed using 3 H Glu as ligand. Results The Kd value of NMDA receptor in hippocampus began to decline immediately after EMP irradiation and decreased most significantly at 3h after irradiation (P <0.05 compared with the control group), gradually recovered at 6h and returned to normal level at 48h. The Bmax of NMDA receptor in hippocampus of irradiated rats decreased significantly at 3h and 6h after irradiation (all P <0. 05), and gradually recovered at 24h after radiotherapy. The Bmax at 48h after irradiation significantly increased , Exceeding the control group (P <0.05). Conclusion EMP radiation can cause NMDA receptor affinity and decreased receptor density in hippocampus of rats. It is suggested that the changes of NMDA receptor density, affinity and excitotoxicity of NMDA Ca2 + NO pathway may be involved in the molecular mechanism of EMP-induced cognitive impairment in experimental animals.