McDonald J W, Silverstein F S, Johnston M V
Neuroscience Training Program, University of Michigan Medical School, Ann Arbor.
Brain Res. 1988 Aug 30;459(1):200-3. doi: 10.1016/0006-8993(88)90306-x.
The neurotoxic lesion produced by direct injection of 25 nmol of N-methyl-D-aspartate (NMDA) into the corpus striatum of 7-day-old rats was compared to the effects of injecting 75 nmol into the striatum or hippocampus of adults. The area of histopathology in the immature striatum was 21 X larger than the striatal lesion in adults. Damage from NMDA injected into the immature striatum also extended into the dorsal hippocampus and produced an area of destruction which was 16 X larger than observed after direct injection into the adult hippocampus. Several studies have implicated excessive N-methyl-D-aspartate receptor activation in the pathogenesis of hypoxic-ischemic and hypoglycemic injury and our results suggest that this neurotoxic mechanism is extremely active in the immature brain.
将25纳摩尔的N-甲基-D-天冬氨酸（NMDA）直接注射到7日龄大鼠的纹状体中所产生的神经毒性损伤，与向成年大鼠的纹状体或海马体中注射75纳摩尔NMDA的效果进行了比较。未成熟纹状体中的组织病理学损伤面积比成年大鼠纹状体中的损伤大21倍。注射到未成熟纹状体中的NMDA造成的损伤还扩展到背侧海马体，产生的破坏区域比直接注射到成年海马体后观察到的大16倍。多项研究表明，N-甲基-D-天冬氨酸受体过度激活与缺氧缺血性和低血糖性损伤的发病机制有关，我们的研究结果表明，这种神经毒性机制在未成熟大脑中极为活跃。
