A lightly platinized tungsten (Pt-W) wire electrode, axially inserted into a crayfish giant axon, causes the development of cardiac-like action potentials with durations of up to 4 s. The plateau in membrane potential typically occurs within 10 min of the start of action potential elongation. The effect occurs without passing current through the Pt-W electrode and is temporally related to a dramatic decrease in intracellular pH (pHi). Such an effect cannot be induced by a decrease in pHi

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... d by equilibrating the axon with HCO3(-)-CO2 solution (pH6), and NH4Cl rebound or direct intracellular injection of PO4(3-) buffer (pH 4 X 5). Action potential elongation is accompanied by a block of delayed rectification and the possibility that inward rectification also develops cannot be ruled out. Plateau generation requires Na+ and Ca2+ inward currents as demonstrated by abolition of the plateau by [Na+]o or [Ca2+]o depletion or treatment with tetrodotoxin (TTX) or verapamil. The block of outward rectification by Pt-W requires external Na+ or Ca2+. Action potential elongation produced by 3,4-diaminopyridine is not sensitive to verapamil and the waveform is different from that produced by Pt-W. The data support the possibility that different classes of excitable membranes have similar channel populations and that the functional differences between them reside in the inhibitory or masking influences that are present in the microenvironments of the various membrane channels.