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目的：研究毒扁豆碱阻断交感节神经元烟碱受体的作用机理．方法：以培养的新生大鼠颈上交感节神经元为标本，使用全细胞膜片箝技术，观察毒扁豆碱对交感节烟碱受体选择性激动剂ＤＭＰＰ诱发电流的影响．结果：毒扁豆碱（５－２０μｍｏｌ·Ｌ－１）以浓度依赖性方式抑制ＤＭＰＰ诱发电流，促进诱发电流的衰减，其抑制作用没有电压依赖性，毒扁豆碱２００μｍｏｌ·Ｌ－１不能激活烟碱受体．结论：与骨骼肌烟碱受体相比，交感神经元烟碱受体表现出不同的药理学特性．毒扁豆碱通过作用于变构位点抑制交感神经元烟碱受体，不影响其开放的离子通道和激动剂结合位点．
OBJECTIVE: To study the mechanism of action of physostigmine in blocking nicotinic receptors in sympathetic ganglion neurons. Methods: Whole-cell patch-clamp technique was used to investigate the effects of physostigmine on the induction of DMPP-induced currents in the sympathetic ganglionic nicotinic receptor. Results: Physostigmine (5-20μmol·L-1) inhibited DMPP-induced currents in a concentration-dependent manner and promoted the decay of induced currents. The inhibitory effect was not voltage-dependent. Physostigmine 200μmol·L-1 could not activate nicotine Receptor. CONCLUSIONS: The sympathetic neuronal nicotinic receptors exhibit different pharmacological properties compared to the nicotinic receptors in skeletal muscle. Physostigmine inhibits the sympathetic neuronal nicotinic receptors by acting on allosteric sites, without affecting its open ion channels and agonist binding sites.