脑损伤后伤侧皮质N-甲基-D-天冬氨酸受体-1表达的变化

Changes of N-methyl-D-aspartate receptor-1 expression in the damaged cortex after brain injury

目的 通过对脑损伤后N-甲基-D-天冬氨酸受体-1 （NMDAR1）表达变化的研究，进一步探讨脑损伤后NMDAR的作用机制。方法 以自由落体致伤方法制作脑损伤模型，以侧脑室注射AP5（2-amino-5-phophonlanoic acid）制作治疗模型，用原位分子杂交技术于不同时间检测伤侧大脑皮质NMDAR1 mRNA表达水平。结果 脑损伤后15 min NMDAR1表达明显增加，伤后72 h 表达最少，伤后168 h 表达基本正常；经AP5治疗，伤后72 h 其表达基本恢复正常。结论 脑损伤后NMDAR1 的过度表达可能参与了继发性脑损害的病理过程，AP5 对脑损伤后神经元具有保护作用。

Objective To investigate the role of a subunit of N-methyl-D-aspartate (NMDAR), a receptor-channel complex, in the neurotoxicity secondary to brain injury and explore its mechanism of action. Methods The animal model of brain injury was established in rats by free-fall metal and the treatment model was induced by injecting AP5 into the lateral ventricle. NMDAR1 mRNA expression levels after brain injury were determined by in situ hybridization. Result NMDAR1 mRNA expression increased significantly at 15 min, utmostly lowered at 72 h and returned to the normal level at 168 h after brain injury. In response to AP5 treatment, NMDAR1 mRNA expression in the treatment group was lower than that in the injured group at 15 min and recovered the normal level at 72 h after brain injury. Conclusion Excessive expression of NMDAR1 mRNA might be involved in the secondary cerebral impairerment after brain injury and the treatment with AP5, a competitive antagonist of NMDAR1, functions to offer neuroprotection.