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

VernacularTitle:脑损伤后伤侧皮质N-甲基-D-天冬氨酸受体-1表达的变化
Author: Cheng-Yi LUO ¹ ; Ru-Xiang XU ; Qing-Hua WANG
Author Information

1. Zhujiang Hospital First Military Medical University
Keywords: brain injury; NMDAR1; expression; 2-aminal-5-phophonlaoicacid
From: Journal of Southern Medical University 2000;20(6):541-541
CountryChina
Language:Chinese
Abstract: 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.