中文摘要：

目的研究NMDA受体甘氨酸位点拮抗剂Y1231对视网膜缺血再灌注损伤后神经节细胞的影响。方法采用视网膜神经节细胞（RGCs）逆行标记，用立体定位仪将大鼠固定，根据大鼠双侧上丘和外侧膝状体在颅骨表面的投影，在投影处钻4个骨孔，每孔注入10g／L的荧光金2μL。2周后采用升高跟压的方法建立大鼠视网膜缺血再灌注模型。将35只SD大鼠随机分为正常对照组（7只），缺血再灌注组（7只）和治疗组（21只）。其中治疗组根据再灌注后不同时间予以0．1％Y12315μL右眼玻璃体腔注射分为1、3、6h组，每组7只大鼠。于再灌注后24h取其视网膜铺片，用荧光显微镜拍照并计算赤道部以内RGCs的数目，对数据进行方差分析。结果缺血再灌注组与治疗组的RGCs数量均少于正常对照组（P〈0．01）。与缺血再灌注组相比，治疗组中1h和3h给药组的RGCs数量明显多（P〈0．01），而6h给药组差异无统计学意义（P=1．0）。结论在视网膜缺血再灌注损伤中，NMDA受体甘氨酸位点拮抗剂Y1231可有效地保护RGCs。

英文摘要：

Objective The increased glutamate in the synaptic cleft following ischemia is thought to play a critical role in the development of neuronal damage. The current studies have demonstrated that several newer glycine site antagonists of the NMDA receptor provide neuroprotection in models of focal cerebral ischemia. The aim of this study was to investigate the effect of NMDA receptors＇ glycine site antagonist Y1231 on retina ganglion cells after retinal ischemia-reperfusion injury. Methods According to the projections of bilateral superior colliculus and lateral geniculate bodies, four bone holes were drilled in 28 SD rats. 2 μL（ 10 g/L）flourogold was injected into the brain via each hole for the labeling of surviving RGCs. Two week later,retinal ischemia was induced in SD rats by increasing intraocular pressure to 110 mmHg through intra-anterior chamber infusion of balance saline solution. 5 μL 0. 1% Y1231 was injected into vitreous of the right eyes of SD model rats in 1,3,6 hours after ischemia-reperfusion respectlvely（7 rats for each time points） ,and 7 normal rats were as control group. Eyeballs of SD rats were enucleated 24 hours after ischemia-reperfusion and whole-mounted retinas were prepared. RGCs within the equator area were counted. Results The RGCs labeled by flourogold showed the golden-yellow fluorescence and no any fluorescence particle was seen in retinal vessel. Compared with normal control group, the number of RGCs was significantly decreased in ischemia- reperfusion group and 0. 1% Y1231 group at different time points （ P 〈 0. 001 ）. In 1 hour and 3 hours after intravitreal injection of 0. 1% Y1231 ,the number of RGCs was significantly increased, but no statistically significant difference was found in 6 hours （P = 1. 000）in comparison with ischemia-reperfuslon group（ P 〈 0. 001 ）. Conclusion NMDA receptors＇ glyclne site antagonist Y1231 can effectively protect retina ganglion cells against retinal ischemla-reperfusion injury.