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目的：研究磷脂酰肌醇代谢对中枢烟碱受体功能的调节作用，以分析脑烟碱受体与磷脂酰肌醇代谢之间的关系．方法：在小鼠上观察肌醇磷酸酶抑制剂氯化锂对烟碱诱发惊厥作用的影响．结果：氯化锂２５－１０ｍｍｏｌ·ｋｇ－１预处理后，烟碱诱发小鼠惊厥的量效关系发生变化，在高于半数效量的剂量下，烟碱诱发惊厥的作用显著增强．但氧颤莫林００５－０２０ｍｇ·ｋｇ－１预处理后，烟碱诱发小鼠惊厥的量效关系无显著变化．在小鼠上每日注射一次氯化锂５０ｍｍｏｌ·ｋｇ－１７ｄ后，烟碱诱发惊厥的作用显著减弱，半数效量由０５８增至０９７ｍｇ·ｋｇ－１．结论：磷脂酰肌醇代谢可调节中枢烟碱受体的功能．
OBJECTIVE: To study the regulatory effect of phosphatidylinositol metabolism on central nicotinic receptor function in order to analyze the relationship between cerebral nicotine receptor and phosphatidylinositol metabolism. Methods: The effects of inositol phosphatase inhibitor lithium chloride on nicotine-induced convulsion in mice were observed. Results: The dose-response relationship of nicotine-induced seizures in mice was pretreated with lithium chloride 25-10mmol · kg-1, and the nicotine-induced seizures increased significantly at higher doses than those of half doses. However, the dose-effect relationship of nicotine-induced convulsions in mice did not change after pretreatment of 0-105-020 mg · kg-1 defaea mint. In mice once daily injection of lithium chloride 5 0mmol · kg-17d, nicotine-induced convulsions significantly weakened, half the effective amount from 0 58 to 0 97mg · kg-1. Conclusion: Phosphatidylinositol metabolism regulates the function of central nicotinic receptors.