Delayed production of nitric oxide contributes to NMDA-mediated neuronal damage.
Delayed production of nitric oxide contributes to NMDA-mediated neuronal damage.
复制标题
一氧化氮产生延迟会导致 NMDA 介导的神经元损伤。
作者：
D. Reif
原代培养的小鼠皮质神经元暴露于N-甲基-D-天冬氨酸(NMDA)可导致神经元死亡，其证据是乳酸脱氢酶(LDH)释放到培养液中。当N-硝基-L-精氨酸(N-Arg)与N-精氨酸同时存在时，N-硝基-L-精氨酸(N-Arg)以浓度依赖的方式保护神经元免于死亡。如果在添加N-精氨酸之前向培养基中添加L-精氨酸，则N-Arg的保护作用消失。在NMDA之前用红藻氨酸处理神经元可以减少随后NMDA引起的损伤，而N-Arg并不能阻止这种损伤。这些结果表明，一氧化氮(NO)的延迟产生参与了NMDA诱导的培养神经元的损伤。
Exposure of primary murine cortical neuron cultures to N-methyl-D-aspartate (NMDA) resulted in neuronal death as evidenced by release of lactate dehydrogenase (LDH) into the media. The addition of N-nitro-L-arginine (N-Arg) protected the neurons from death in a concentration-dependent manner when added after the NMDA, but not when the N-Arg was present with the NMDA. Protection by N-Arg was lost if L-arginine containing media was added to the cultures prior to the addition of the N-Arg. Treatment of the neurons with kainate prior to NMDA reduced subsequent NMDA-induced damage which was not prevented with N-Arg. These results suggest that delayed production of nitric oxide (NO) contributes to NMDA-induced neuronal damage in culture.