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目的旨在进一步阐明阿片依赖中ＰＬＣＰＫＣ信号系统的变化与作用。用小鼠吗啡依赖模型，观察脑组织磷酸肌醇含量、ＰＫＣ活性变化。结果发现：纹状体ＩＰ及ＩＰ３、大脑皮质ＩＰ含量明显升高，二者磷酸肌醇总量显著增加；胞质可溶相ＰＫＣ活性在大脑皮质及小脑明显升高，在纹状体显著下降。膜相ＰＫＣ活性在纹状体明显升高，在小脑和海马明显降低；ＰＫＣ抑制剂可抑制吗啡依赖的产生。结果提示，吗啡依赖小鼠纹状体磷酸肌醇含量的增加意味着ＰＬＣ的活化，这可能与纹状体中ＰＫＣ的激活有关，而该ＰＫＣ的激活可能参与吗啡依赖的形成
The purpose is to further elucidate the changes and effects of PLC-PKC signaling system in opioid dependence. Mice morphine dependence model was used to observe the changes of phosphoinositide content and PKC activity in brain tissue. The results showed that the IP content of striatum in IP and IP3 and cerebral cortex were significantly increased, and the total amount of phosphoinositides in both groups was significantly increased. PKC activity in cytoplasm soluble phase was significantly increased in cerebral cortex and cerebellum and significantly decreased in striatum . Membrane PKC activity in the striatum was significantly increased in the cerebellum and hippocampus significantly reduced; PKC inhibitors can inhibit morphine-dependent production. The results suggest that the increase of phosphoinositide level in striatum of morphine dependent mice implies activation of PLC, which may be related to the activation of PKC in striatum, and the activation of PKC may be involved in the morphine-dependent formation