The effects of the compounds 2-, 3- and 4-aminopyridine and sparteine on membrane conductance changes were examined using both voltage-clamped Myxicola axons and the lobster [Homarus americanus] neuromuscular junction. In Myxicola axons, the aminopyridines specifically inhibited K conductance when applied at concentrations of 0.1-5 mM without any apparent effect of resting membrane potential. Concentrations in excess of 5 mM were needed to inhibit Na conductance noticeably. K conductance-voltage curves were shifted in the depolarized direction along the voltage axis with no significant change in shape. There were only minor changes in the kinetics of K activation. In high K solutions, both inward and outward K currents were equally sensitive to the aminopyridines. Sparteine was generally a more potent but somewhat less specific inhibitor of K conductance. In contrast to the aminopyridines, sparteine was more effective when applied at basic pH and in addition tended to produce a noticeable degree of K inactivation. When applied to the lobster neuromuscular junction, 2-aminopyridine and sparteine dramatically increased the amplitude of excitatory and inhibitory postjunctional potentials, with little or no change in resting potential, resting input conductance, reversal potential or miniature end plate potential amplitude or frequency. Quantal content per fiber was increased by a factor of .apprx. 3 for excitatory responses.