Physostigmine blocked nicotinic acetylcholine receptors in rat sympathetic ganglion neurons

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．

IM: To study the blocking mechanism of physostigmine (Phy) on nicotinic acetylcholine receptors (NAChR) in sympathetic neurons. METHODS: The whole cell patch clamp technique was used to observe the effects of Phy on NAChR in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG). RESULTS: Phy 5-20 μmol·L -1 inhibited neuronal NAChR in a concentration dependent manner and accelerated the desensitization of NAChR. Changing the membrane potential from -50 to -90 mV did not affect the blocking effect of Phy. Phy 200 μmol·L -1 did not induce any noticeable response in SCG neurons. CONCLUSION: Phy blocked NAChR in the sympathetic ganglion neurons by interacting with the allosteric sites out of the binding sites and the open ionic channels of the receptors. Phy did not possess excitative effect on NAChR in SCG neurons.