Reif D W
Biology Department, Fisons Pharmaceuticals, Rochester, NY 14603.
Neuroreport. 1993 May;4(5):566-8. doi: 10.1097/00001756-199305000-00026.
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.
将原代小鼠皮质神经元培养物暴露于N-甲基-D-天冬氨酸（NMDA）会导致神经元死亡，这可通过培养基中乳酸脱氢酶（LDH）的释放得到证明。当在NMDA之后添加N-硝基-L-精氨酸（N-Arg）时，它以浓度依赖的方式保护神经元免于死亡，但当N-Arg与NMDA同时存在时则不然。如果在添加N-Arg之前向培养物中添加含L-精氨酸的培养基，则N-Arg的保护作用会丧失。在NMDA之前用红藻氨酸处理神经元可减少随后NMDA诱导的损伤，而N-Arg不能预防这种损伤。这些结果表明，一氧化氮（NO）的延迟产生会导致培养物中NMDA诱导的神经元损伤。
