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为探索谷氨酸受体（GluR）在介导谷氨酸（Glu）对缺血神经元损伤的作用机制，本实验建立大鼠大脑中动脉阻塞（MCAO）局部脑缺血实验模型，应用受体的放射配基结合分析（RBA）等技术动．态监测了缺血及再灌流期缺血灶、海马和下丘脑Glu、GluR含量及其亲和力的变化。结果发现：缺血30min，各脑区Glu含量达高峰，再灌流6h，Glu含量回降至基线水平，再灌流48h后，Glu含量再次中等程度升高，并持续至再灌流72h。GluR和KD值与Glu含量密切相关。结果提示，缺血再灌流早期，GluR在高浓度Glu的作用下发生同种特异性反向调节，GluR亲和力为增敏反应；再灌流中晚期，GluR的变化属于同种特异性正向调节，而GluR亲和力测为减敏反应。
In order to explore the role of glutamate receptor (GluR) in mediating the effect of glutamate (Glu) on ischemic neuronal damage, we established a rat model of middle cerebral artery occlusion (MCAO) Body radioligand binding analysis (RBA) and other technologies. The levels of Glu and GluR in ischemic, hippocampal and hypothalamus during ischemia and reperfusion were monitored. The results showed that the content of Glu reached the peak at 30 min after ischemia, and the content of Glu decreased to the baseline level at 6 h after reperfusion. After 48 h of reperfusion, the content of Glu increased again moderately until reperfusion for 72 h. GluR and KD values are closely related to Glu content. The results suggest that GluR at the early stage of ischemia-reperfusion in the high concentration of Glu under the same kind of specific reverse regulation, GluR affinity for the sensitization response; reperfusion in the late, GluR changes belong to the same type of specific positive regulation, GluR affinity was measured as a desensitization reaction.