李玉红，李锦，苏瑞斌，吴宁，李子建，王水明，彭瑞云，王德文.电磁脉冲对大鼠海马N-甲基-D-天门冬氨酸受体活性的影响[J].中华物理医学与康复杂志,2004,(7):
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| 电磁脉冲对大鼠海马N-甲基-D-天门冬氨酸受体活性的影响 |
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| DOI： |
| 中文关键词: 电磁脉冲 N-甲基-D-天门冬氨酸受体 海马 放射性配基受体结合实验 |
| 英文关键词: Electromagnetic pulse N-methyl-D-aspartate receptor Hippocampus Ridioligand binding assay |
| 基金项目:全军医药卫生指令性课题（No.01L023） |
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| 中文摘要: |
| 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6×104V/m,脉冲上升时间20 ns，脉宽30 μs，频率2.5脉冲/min，作用2 min。二级雄性Wistar大鼠32只，随机分为EMP组（n=26）和对照组（n=6）。EMP组大鼠分别于辐射后即刻,3 h,6 h,24 h和48 h断头取脑，剥离海马，制备膜受体蛋白，以3H-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3 h下降最显著（与对照组相比，P＜0.05），6 h渐有恢复，48 h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3 h和6 h显著下降（与对照组相比，均P＜0.05），24 h渐有恢复，辐射后48 h Bmax值明显升高，超过对照组水平(P＜0.05）。 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。 |
| 英文摘要: |
| Objective To investigate the relationship between the changes of N-methyl-D-aspartate(NMDA) receptor activity in hippocampus of rats and electromagnetic pulses(EMP) exposure. MethodsThirty-two rats were divided into a control group (6 rats) and an experimental group (26 rats), subject to EMP irradiation. The rats in the experimental group were decapitated after EMP(6×104V/m,rise time 20ns,pulse width 30μs,5 pulses in 2 minutes) irradiation and hippocampus were sampled, and NMDA receptor activity were detected with a radioligand binding assay with 3H-Glu. The rats in the control group were treated the same except EMP exposure. ResultsThe Kd value of NMDA receptor decreased significantly at 3h after irradiation, then increased gradually after 6h and reached normal level at 48h after irradiation. The Bmax value of the receptor decreased significantly at 3~6h after exposure, then began to rise at 24h and reached a higher level than that of the control group. ConclusionEMP irradiation induced the decrease of both Kd and Bmax values of NMDA receptors in hippocampus of rats. It was suggested that the changes of density and affinity of NMDA receptor might be partly responsible for the cognitive deficits of rats. |
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