吗啡处理组 (10mg·kg-1,sc)和吗啡依赖组大鼠脊髓鸟苷酸环化酶 (GC)基础活力和氧化氮 (硝普钠为供体 )刺激酶活力升高 ,cGMP含量却降低。纳络酮处理后 ,依赖大鼠脊髓GC活力降低 ,对NO敏感性提高 ,cGMP含量剧升。M受体激动剂氨甲酰胆碱可抑制对照组和吗啡处理组脊髓GC活力 ,对吗啡依赖以及纳洛酮处理组的GC抑制作用消失。结果表明脊髓GC对氧化氮和M受体激动剂的反应性改变在吗啡依赖及戒断反应中起重要作用。 Morphine-treated group (10 mg · kg-1, sc) and morphine-dependent group rats spinal cord guanylate cyclase (GC) basic activity and nitric oxide (sodium nitroprusside donor) stimulated enzyme activity, cGMP content reduce. Naloxone treatment, dependent on GC spinal cord activity was decreased, increased sensitivity to NO, cGMP levels soared. M receptor agonist carbachol inhibited GC activity of spinal cord in the control and morphine treated groups, but disappeared in the morphine dependent and naloxone treated groups. The results show that spinal GC changes in reactivity to nitric oxide and M receptor agonists play an important role in morphine dependence and withdrawal response.