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采用体外实验研究烟碱对大鼠脑Ｍ受体信息跨膜转导的调节作用．脑突触体以烟碱１．０μｍｏｌ·Ｌ－１预处理后，［３Ｈ］ｌ－二苯羟乙酸奎宁酯与Ｍ受体结合及解离动力学过程减慢．在溶脱的大脑皮层Ｍ受体与Ｇ蛋白复合体上，烟碱１．０μｍｏｌ·Ｌ－１可减慢［３５Ｓ］－腺苷５＇－［γ－硫］三磷酸与Ｇ蛋白的结合，并增强Ｍ受体与Ｇ蛋白之间的偶联关系．烟碱０．１～１０００μｍｏｌ·Ｌ－１既不影响纹状体腺苷酸环化酶的基础活性，也不影响氟化钠激活腺苷酸环化酶的作用．烟碱０．１～３０μｍｏｌ·Ｌ－１浓度依赖性地提高脑细胞内Ｃａ２＋浓度．据此提出烟碱对脑Ｍ受体信息跨膜转导系统有多点调节作用．
In vitro study of nicotine on the regulation of M receptor transmembrane transduction in rat brain. Brain synaptosome pretreatment with nicotine 1.0μmol·L-1, [3H] l-benzidine and M receptor binding and dissociation kinetics slowed down. Nicotine 1.0 μmol·L -1 slows the binding of [35 S] -adenosine 5 ’- [γ-thio] triphosphate to G protein in the stripped cortex M receptor and G protein complex Enhances the coupling between M receptor and G protein. Nicotine 0.1 ~ 1000μmol·L-1 did not affect basal activity of striatal adenylate cyclase nor did sodium fluoride activate adenylate cyclase. Nicotine 0.1 ~ 30μmol·L-1 concentration-dependently increased intracellular Ca2 + concentration. Accordingly, nicotine is suggested to regulate the M transmembrane transduction system of brain M receptor.