The n-alcohols butanol through nonanol and the volatile anesthetic ether increase the frequency of bursts of nicotinic acetylcholine (ACh) receptor channels induced by low concentrations of agonists. For example, 10 mM butanol increases the burst frequency induced by 0.2 microM ACh (a full agonist) and 1 microM decamethonium (a partial agonist) by 1.6-fold and 2.7-fold, respectively. An increase in burst frequency could arise from effects of the drug on agonist binding, channel gating, or desensitization. To distinguish among these alternatives, we measured the current response to rapid application of saturating concentrations of agonists. We found that 10 mM butanol increases the peak current induced by 100 microM decamethonium by 2-fold. In addition, 20 mM butanol and 3 mM pentanol both decrease the onset time of the current response to 10 mM ACh by about 40%. In contrast, ether does not increase the current response to 100 microM decamethonium and does not significantly change the onset time for 10 mM ACh. Neither ether nor butanol changes the degree of steady state desensitization induced by 0.2 microM ACh. We conclude that butanol and pentanol increase burst frequency by increasing the channel opening rate, whereas ether does so by increasing the agonist binding affinity of the ACh receptor.