Alkadhi K, Branisteanu D D, Henderson E G, Lambert J J, Volle R L
Naunyn Schmiedebergs Arch Pharmacol. 1980 Jun;312(2):117-21. doi: 10.1007/BF00569719.
The muscarinic ganglion stimulating agent, McN-A-343 has unusual blocking actions on endplate currents (EPCs) at frog neuromuscular junctions. McN-A-343 caused depolarization by a curare-sensitive process, blocked neuromuscular transmission, depressed EPCs and reduced the time for EPC decay. These results are explained best by a nicotinic agonist action of McN-A-343 on the acetylcholine receptor to cause ion flow and the blockade by McN-A-343 of the open ion channels. The actions of McN-A-343 are similar to those of decamethonium (C-10) described by others. Unlike C-10, however, McN-A-343 did not alter the exponential character of the EPC or alter the voltage dependency of the EPC. The prototypical nicotinic agonist, dimethylphenylpiperazinium had no effect on EPC parameters of endplate clamped at -90mV.
毒蕈碱型神经节刺激剂 McN-A-343 对青蛙神经肌肉接头处的终板电流（EPCs）具有不同寻常的阻断作用。McN-A-343 通过箭毒敏感过程引起去极化，阻断神经肌肉传递，抑制 EPCs 并缩短 EPC 衰减时间。这些结果最好用 McN-A-343 对乙酰胆碱受体的烟碱样激动剂作用来解释，该作用导致离子流动以及 McN-A-343 对开放离子通道的阻断。McN-A-343 的作用与其他人描述的十烃季铵（C-10）的作用相似。然而，与 C-10 不同的是，McN-A-343 并未改变 EPC 的指数特性，也未改变 EPC 的电压依赖性。典型的烟碱样激动剂二甲基苯基哌嗪对钳制在 -90mV 的终板的 EPC 参数没有影响。
