目的　观察阿片类依赖时Ca2 + 钙调蛋白依赖的蛋白激酶II信息通路的变化。方法　以NG10 8 15细胞作为体外的细胞模型 ,分别用竞争性蛋白结合法及放射免疫法、PDE法、γ 32 P参入法测定cAMP水平、钙调蛋白(CaM)活性和钙调蛋白依赖的蛋白激酶II(CaMKII)活性。结果　DPDPE作用NG10 8 15细胞 48h可使细胞浆和细胞核CaM和CaMKII活性升高 ,该变化可被CaM特异性拮抗剂W 7所抑制 ;CaMKII特异性抑制剂KN 6 2可抑制CaMKII活性的增高 ,而对CaM活性无明显影响。DPDPE作用NG10 8 15细胞 48h后 ,加入纳洛酮 ,CaM活性、CaMKII活性进一步增高。结论　Ca2 + CaMKII信息通路参与了阿片依赖的机制。 Objective To observe the changes of Ca2 + calmodulin-dependent protein kinase II (IGF-II) pathway during opioid dependence. Methods NG10 8 15 cells were used as a cell model in vitro. The levels of cAMP, calmodulin (CaM) and calmodulin-dependent protein were determined by competitive protein binding assay, radioimmunoassay, PDE assay and γ 32 P incorporation, respectively Kinase II (CaMKII) activity. Results DPDPE induced the activity of CaM and CaMKII in cytoplasm and nucleus at 48h in NG10 8 15 cells, which could be inhibited by the CaM-specific antagonist W 7. The specific inhibitor of CaMKII KN 6 2 could inhibit the increase of CaMKII activity, While no significant effect on CaM activity. DPDPE treated NG10 8 15 cells 48h, adding naloxone, CaM activity, CaMKII activity further increased. Conclusion Ca2 + CaMKII signaling pathway is involved in opioid dependence.