Current evidence indicates that glutamate acting via the N-methyl-D-aspartate (NMDA) receptor/ion channel complex plays a major role in the neuronal degeneration associated with a variety of neurological disorders. In this report the role of glycine in NMDA neurotoxicity was examined. We demonstrate that NMDA-mediated neurotoxicity is markedly potentiated by glycine and other amino acids, e.g., D-serine. Putative glycine antagonists HA-966 and 7-chlorokynurenic acid were highly effective in preventing NMDA neurotoxicity, even in the absence of added glycine. The neuroprotective action of HA-966 and 7-chlorokynurenic acid, but not that of NMDA antagonists 3-(2-carboxypiperazine-4-yl)propylphosphonate and MK-801, could be reversed by glycine. These results indicate that glycine, operating through a strychinine-insensitive glycine site, plays a central permissive role in NMDA-mediated neurotoxicity.

译文

目前的证据表明,通过N-甲基-D-天冬氨酸 (NMDA) 受体/离子通道复合物起作用的谷氨酸在与多种神经系统疾病相关的神经元变性中起主要作用。在本报告中,研究了甘氨酸在NMDA神经毒性中的作用。我们证明了NMDA介导的神经毒性被甘氨酸和其他氨基酸 (例如D-丝氨酸) 显着增强。假定的甘氨酸拮抗剂HA-966和7-氯核糖核酸在预防NMDA神经毒性方面非常有效,即使在没有添加甘氨酸的情况下也是如此。甘氨酸可以逆转HA-966和7-氯代尿酸的神经保护作用,而非NMDA拮抗剂3-(2-羧基哌嗪-4-基) 丙基膦酸盐和MK-801的神经保护作用。这些结果表明,甘氨酸通过对士林不敏感的甘氨酸位点起作用,在NMDA介导的神经毒性中起着中心许可作用。

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