中文摘要：

①目的探讨NMDA受体甘氨酸位点拮抗剂的士宁（strychnine）及其与MK801共同作用在大鼠海马CA1区缺血性神经元损伤中的作用。②方法健康成年雄性SD大鼠制作4动脉闭塞全脑缺血模型,实验动物随机分为Sham、溶剂对照（Vehicle）组（I/R＋Sa-line）、MK801组（I/R＋MK801）及strychnine和MK801共同作用组（I/R＋Glycine＋strychnine＋MK801）。观察海马CA1区生存神经元。利用Morris水迷宫观察脑缺血再灌注后大鼠的空间学习记忆功能的变化情况。③结果与缺血再灌注组相比,strychnine和MK801共同作用组海马CA1区神经元生存数量明显增加;大鼠缺血后的空间学习记忆缺陷明显得到改善。④结论 NMDA受体甘氨酸位点拮抗剂strychnine和MK801共同作用可有效减轻大鼠缺血再灌注后神经元损伤,为临床治疗缺血性脑中风提供理论依据。

英文摘要：

Objective The goal of this study was to elucidate the role of strychnine and MK801 following global cerebral ischemia in hippocampal CA1 region.Methods Adult male Sprague-Dawley rats were subjected to global cerebral ischemia by four-vessel occlusion.Experimental animals were randomly divided into four groups,sham,ischemia-reperfusion（I/R）,Glycine（I/R ＋ Saline）,MK801（I/R ＋ MK801） and strychnine and MK801（I/R ＋Glycine＋ strychnine＋MK801）groups.The spatial learning and memory ability of the rats was monitored by the Morris Water Maze.Results Compared with ischemia-reperfusion groups,treatment with Glycine＋ strychnine＋MK801 significantly increased the number of survivaling neurons in hippocampal CA1 region and markedly improved the ability of spatial learning and memory of the rats following ischemic injury.Conclusion strychnine might be an important mechanism in neuronal injury response to global ischemic-reperfusion.