Mikuni N, Babb T L, Christi W
Department of Neurosciences, The Cleveland Clinic Foundation, OH 44195, USA.
Neurosci Lett. 1999 Jun 4;267(3):165-8. doi: 10.1016/s0304-3940(99)00355-9.
The N-methyl-D-aspartate receptors (NMDAR) produce physiologically functional channels for enhanced excitatory neurotransmission when they exist as heteromeric complexes containing the NMDAR1 subunit combined with NMDAR2. We examined the expressions of NMDAR1 and 2A/B protein in the kainic acid induced rat chronic epileptic hippocampus. Immunoreactivities of both NMDAR1 and NDMAR2A/B were increased in the inner molecular layer of the dentate gyrus, while they were decreased in the hilar and CA3/4 pyramidal zones. Immunoblot analysis demonstrated that the overall level of NMDAR1-2A/B coassembly was increased in the whole hippocampus. These results indicate that the increase of the NMDAR1-2A/B complex in the inner molecular layer is a significant cellular mechanism that contributes to focal hyperexcitability in rat chronic hippocampal epilepsy.
N-甲基-D-天冬氨酸受体（NMDAR）在作为包含NMDAR1亚基与NMDAR2结合的异源复合物存在时，会产生用于增强兴奋性神经传递的生理功能通道。我们检测了在 kainic 酸诱导的大鼠慢性癫痫海马体中NMDAR1和2A/B蛋白的表达。NMDAR1和NDMAR2A/B在齿状回内分子层的免疫反应性均增加，而在门区和CA3/4锥体区则降低。免疫印迹分析表明，整个海马体中NMDAR1-2A/B共组装的总体水平增加。这些结果表明，内分子层中NMDAR1-2A/B复合物的增加是导致大鼠慢性海马癫痫局灶性兴奋性过高的重要细胞机制。
