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The apparent lifetimes of frog end-plate channels activated by several nicotinic agonists have been determined with voltage-jump and fluctuation analysis techniques. The agonists were monoquaternary, N-substituted derivatives of trimethylammonium (TMA). Methyl TMA activated channels which had apparent lifetimes about 3-4 times shorter than acetylcholine (ACh)-activated channels. This result was confirmed with single-channel recordings from embryonic chick skeletal muscle. Channel conductance and voltage dependence of channel lifetime were similar for methyl TMA- and ACh-activated channels. Methyl TMA showed no signs of blocking open end-plate channels. Ethyl TMA, acetylthiocholine, cholinethiol and carbamylcholine all activated channels similar to methyl TMA-activated channels with regard to lifetime. None of these agonists appeared to block end-plate channels in the employed concentrations. 4-ketopentyl TMA, which contains a methylene group in place of the ether oxygen of ACh, sometimes opened end-plate channels with similar apparent lifetimes as those opened by ACh. Single-channel recordings showed that bursts of current from channels activated by 4-ketopentyl TMA have similar durations as do those activated by ACh. Pentyl TMA and benzyl TMA block open end-plate channels even when delivered at doses which elicit very small currents. It is concluded that the ester moiety of ACh serves to stabilize the open conformation of the channel.