NMDA受体与癫痫发病机制的研究现状

被引:5
作者
来海欧
杨金升
机构
[1] 兰州军区兰州总医院神经内科
关键词
N-甲基-D-天门冬氨酸受体; N-甲基-D-冬氨酸受体亚单位2B阻滞剂; 艾芬地尔; 发病机制;
D O I
10.16636/j.cnki.jinn.2008.01.011
中图分类号
R742.1 [癫痫];
学科分类号
1002 ;
摘要
癫痫的主要机制为脑内兴奋性氨基酸活性升高。在癫痫发作中,N-甲基-D-天门冬氨酸(NMDA)受体含量增多,表达升高,且其各个亚型之间相互作用,构形发生变化,使突触后膜支架蛋白磷酸化,发生级联发应,使NMDA受体配体离子通道持续开放,神经元持续放电,并向周围神经元放散扩布;长期癫痫反复发作,导致苔藓纤维发芽,神经元缺失;这些形态学和电生理改变,反之,导致癫痫的易感和反复发作。通过多年动物实验和临床应用,提示N-甲基-D-冬氨酸受体亚单位2B(NR2B),高选择性的拮抗剂有广阔的临床应用前景。
引用
收藏
页码:72 / 76
页数:5
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