Wood E R, Bussey T J, Phillips A G
Department of Psychology, University of British Columbia, Vancouver, Canada.
Neuroreport. 1993 Feb;4(2):151-4. doi: 10.1097/00001756-199302000-00009.
Transient global ischemia can result in permanent neuronal damage and impairments in learning and memory. We investigated the therapeutic potential of 7-Chlorokynurenic acid, a potent antagonist at the glycine-modulatory site on the NMDA receptor, in terms of both neuroprotection and behavioral outcome in rats following transient forebrain ischemia. Intraventricular administration of the drug immediately before ischemia significantly attenuated ischemia-induced CA1 pyramidal cell loss. Moreover, ischemic rats treated with 7-Chlorokynurenic acid showed unimpaired acquisition of a delayed nonmatching to sample task 8 weeks following surgery, whereas saline-treated ischemic rats were significantly impaired. These data provide preliminary evidence that the glycine site may be an appropriate target for therapeutic agents in ischemia.
短暂性全脑缺血可导致永久性神经元损伤以及学习和记忆障碍。我们研究了7-氯犬尿氨酸（一种NMDA受体甘氨酸调节位点的强效拮抗剂）在短暂性前脑缺血大鼠中的神经保护作用和行为学结果方面的治疗潜力。在缺血前立即脑室内注射该药物可显著减轻缺血诱导的CA1锥体细胞损失。此外，用7-氯犬尿氨酸治疗的缺血大鼠在手术后8周进行的延迟非匹配样本任务中学习未受损害，而用生理盐水治疗的缺血大鼠则明显受损。这些数据提供了初步证据，表明甘氨酸位点可能是缺血治疗药物的合适靶点。
