Wood E R, Bussey T J, Phillips A G
Department of Psychology, University of British Columbia, Vancouver, Canada.
Neurosci Lett. 1992 Sep 28;145(1):10-4. doi: 10.1016/0304-3940(92)90191-9.
Excessive activation of the N-methyl-D-aspartate (NMDA) receptor-channel complex has been implicated as one of the mechanisms by which ischemia-induced neuronal damage is mediated. Elevated glycine levels during ischemia may contribute to damage mediated by the NMDA receptor as glycine binding potentiates NMDA responses, and may be necessary for channel opening. We investigated the protective effects of 7-chlorokynurenic acid--a competitive antagonist at the glycine binding site associated with the NMDA receptor--against hippocampal CA1 cell loss induced by transient forebrain ischemia in rats. Intraventricular administration of the drug immediately before the onset of ischemia significantly attenuated neuronal loss compared to vehicle-treated animals.
N-甲基-D-天冬氨酸（NMDA）受体通道复合物的过度激活被认为是介导缺血性神经元损伤的机制之一。缺血期间甘氨酸水平升高可能导致由NMDA受体介导的损伤，因为甘氨酸结合会增强NMDA反应，并且可能是通道开放所必需的。我们研究了7-氯犬尿氨酸（一种与NMDA受体相关的甘氨酸结合位点的竞争性拮抗剂）对大鼠短暂性前脑缺血诱导的海马CA1细胞丢失的保护作用。与给予赋形剂处理的动物相比，在缺血发作前立即脑室内给药该药物可显著减轻神经元丢失。
