Neely A, Lingle C J
Biophys J. 1986 Nov;50(5):981-6. doi: 10.1016/S0006-3495(86)83538-X.
At the ganglionic nicotinic acetylcholine channel (Gurney, A. M., and H. P. Rang, 1984, Br. J. Pharmacol., 82:623-642) and on some cholinergic neuromuscular synapses of Crustacea (Lingle, C., 1983a, J. Physiol. (Lond.), 339:395-417; Lingle, C., 1983b, J. Physiol. (Lond.), 339:419-437), some agents that block cholinergic currents by an open-channel block mechanism appear to become trapped within the channel when it subsequently closes. It is unknown whether trapping of some open-channel blockers might also occur at the neuromuscular nicotinic acetylcholine channel. Here we show that the long-lived cholinergic blocking action of chlorisondamine, a ganglionic nicotinic blocker, can in part be most simply explained by an open-channel block mechanism followed by a subsequent trapping of the blocking molecule within the closed ion channel. Unique structural characteristics of the chlorisondamine molecule place several provocative constraints on the mechanism by which trapping may be occurring.
在神经节烟碱型乙酰胆碱通道（格尼，A.M.，和H.P. 兰格，1984年，《英国药理学期刊》，82:623 - 642）以及某些甲壳纲动物的胆碱能神经肌肉突触上（林格尔，C.，1983a，《生理学杂志》（伦敦），339:395 - 417；林格尔，C.，1983b，《生理学杂志》（伦敦），339:419 - 437），一些通过开放通道阻断机制来阻断胆碱能电流的药物，当通道随后关闭时，似乎会被困在通道内。尚不清楚在神经肌肉烟碱型乙酰胆碱通道是否也会发生一些开放通道阻断剂的被困现象。在此我们表明，神经节烟碱型阻断剂氯异吲哚铵的长效胆碱能阻断作用，部分可以最简单地通过开放通道阻断机制来解释，随后阻断分子被困在关闭的离子通道内。氯异吲哚铵分子独特的结构特征对可能发生被困的机制施加了几个具有启发性的限制条件。
