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采用四动脉闭塞全脑缺血模型，观察大鼠缺血３０ｍｉｎ再灌注２１ｄ不同时间中，外源性谷氨酸（Ｇｌｕ）对海马脑片磷脂酰肌醇（ＰＩ）代谢的影响和偶联该系统的Ｇ蛋白功能变化。结果显示，Ｇｌｕ（５００μｍｏｌ／Ｌ）对正常和缺血再灌注海马脑片肌醇磷酸（ＩＰ）生成均具明显的促进作用（Ｐ＜０．０１，ｎ＝９），其中以缺血再灌注后ＩＰ的升高为显著，并且这种Ｇｌｕ刺激的ＩＰ堆积效应随缺血再灌注时间的延长在２１ｄ中持续存在。与此同时，还观察到缺血再灌注２４ｈ至７ｄ中，海马神经元Ｇｌｕ受体密度（Ｂｍａｘ）显著下降（Ｐ＜０．０１，ｎ＝８），亲和力（Ｋｄ）无显著变化。提示脑缺血再灌注后Ｇｌｕ刺激的ＰＩ代谢增强是由于Ｇｌｕ受体与磷脂酶Ｃ（ＰＬＣ）间产生高反应所致。应用四氟化铝（ＡｌＦ＿４￣－）可得到与上述Ｇｌｕ刺激ＩＰ生成相同的结果，而氨甲酰胆碱（Ｃａｈ）和去甲肾上腺素（ＮＥ）对ＩＰ水平的作用不受脑缺血和再灌注的影响。表明缺血状态下的这种Ｇｌｕ与ＰＬＣ间的高反应可能是特异的，并通过偶联该系统的Ｇ蛋白功能变化介导。
The model of global cerebral ischemia with four-artery occlusion was used to observe the effect of glutamate (Glu) on the metabolism of phosphatidylinositol (PI) in rat hippocampal slices at different time points after ischemia 30min and 21d System of G protein function changes. The results showed that Glu (500μmol / L) significantly promoted the formation of inositol phosphate (IP) in hippocampal slices of normal and ischemia reperfusion rats (P <0.01, n = 9) After IP increased significantly, and this accumulation of Glu-stimulated effect with the extension of ischemia-reperfusion time persists in 21d. At the same time, it was also observed that the Glu receptor density (Bmax) of hippocampal neurons decreased significantly (P <0.01, n = 8) and the affinity (Kd) did not change from 24h to 7d after ischemia / reperfusion. It is suggested that the increase of Glu-stimulated PI metabolism after cerebral ischemia-reperfusion is due to the high reaction between Glu receptor and phospholipase C (PLC). The same results were obtained with aluminum tetrafluoride (AlF 4 ~-) as described above for Glu-stimulated IP production, whereas the effects of carbachol (Cah) and norepinephrine (NE) on IP levels were not affected by cerebral ischemia and Reperfusion effects. This suggests that this high level of Glu-PLC response to ischaemia may be specific and mediated through functional changes in the G protein coupled to the system.