Intra-axonal recordings were obtained from myelinated axons innervating a lizard skeletal muscle. Bath application of tetraethylammonium (TEA, 1-10 mM) depolarized the resting potential, prolonged the action potential and increased the amplitude and duration of the ensuing passive depolarizing after-potential (DAP) in a dose-dependent and reversible manner. TEA increased the axonal input resistance and the slow time constant of the passive voltage response, not only in depolarized axons, but also in resting and hyperpolarized axons. The resting input resistance was tripled in 10 mM-TEA. TEA's effects on the resting potential and action potential usually approached a steady state within 5 min, whereas TEA's effects on input resistance and on the amplitude and time course of the DAP increased progressively for 10-15 min or more, and persisted for 10-15 min after removal of TEA from the bath. 4-Aminopyridine (4-AP, 1 mM), which prolonged the action potential by about the same extent as 10 mM-TEA, did not depolarize the resting potential or increase the resting input resistance, and produced a much smaller increase in DAP time course than 10 mM-TEA. Gallamine (1 mM) had effects more similar to those of TEA. These results suggest that the resting input conductance and DAP time course in lizard motor axons are controlled in part by K+ channels that are blocked by TEA and gallamine, but not by 4-AP. The slow development of the TEA-induced increase in input resistance and DAP time course suggests that some of these channels are located in paranodal or internodal axolemma. In TEA and gallamine additional depolarizing potentials were superimposed on the falling phase of the action potential and on the passive DAP. These superimposed potentials were abolished by 1 mM-Mn2+, and were probably caused by Ca2+ influx into motor terminals.
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