Objective: To investigate the relationship between the changes of N methyl D aspartate (NMDA) receptor activity and brain edema after injury in rats. Methods: The brain injury models were made by using a free falling ...Objective: To investigate the relationship between the changes of N methyl D aspartate (NMDA) receptor activity and brain edema after injury in rats. Methods: The brain injury models were made by using a free falling body. The treatment model was induced by means of injecting AP5 into lateral ventricle before brain injury; water contents in brain cortex were measured with dry wet method; and NMDA receptor activity was detected with a radio ligand binding assay. Results: The water contents began to increase at 30 minutes and reached the peak at 6 hours after brain injury. The maximal binding (B max ) of NMDA receptor increased significantly at 15 minutes and reached the peak at 30 minutes, then decreased gradually and had the lowest value 6 hours after brain injury. Followed the treatment with AP5, NMDA receptor activity in the injured brain showed a normal value; and the water contents were lower than that of AP5 free injury group 24 hours after brain injury. Conclusions: It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the secondary cerebral impairments, and AP5 may protect the brain from edema after brain injury.展开更多
基金NaturalScienceFoundationofGuangdong Province (GD990 416 )NaturalScienceFoundationofChina(39770 76 0 )
文摘Objective: To investigate the relationship between the changes of N methyl D aspartate (NMDA) receptor activity and brain edema after injury in rats. Methods: The brain injury models were made by using a free falling body. The treatment model was induced by means of injecting AP5 into lateral ventricle before brain injury; water contents in brain cortex were measured with dry wet method; and NMDA receptor activity was detected with a radio ligand binding assay. Results: The water contents began to increase at 30 minutes and reached the peak at 6 hours after brain injury. The maximal binding (B max ) of NMDA receptor increased significantly at 15 minutes and reached the peak at 30 minutes, then decreased gradually and had the lowest value 6 hours after brain injury. Followed the treatment with AP5, NMDA receptor activity in the injured brain showed a normal value; and the water contents were lower than that of AP5 free injury group 24 hours after brain injury. Conclusions: It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the secondary cerebral impairments, and AP5 may protect the brain from edema after brain injury.
