Effect of batrachotoxin on the electroplax of electric eel: evidence for voltage-dependent interaction with sodium channels.

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Abstract
Batrachotoxin from the skin of Phyllobates aurotaenia under certain conditions had a strong depolarizing effect on the innervated membrane of the monocellular electroplax preparation from the electric eel, Electrophorus electricus. No effect was observed when the toxin (50-200 nM) was applied to the resting membrane for periods up to 1 h. If the membrane was exposed to batrachotoxin and the cell was subjected to stimulation at a stimulus voltage slightly above the threshold for action potential firing, a progressive prolongation of the action potential and concomitant progressive depolarization of the innervated membrane was observed. When the membrane was depolarized by 15-20 mV, a further abrupt all-or-none depolarization occurred, and the potential attained a steady-state value between 0 and -10 mV. Brief stimulation of a cell in the presence of batrachotoxin was sufficient to define a batrachotoxin-treated cell, even though negligible depolarization occurred. If depolarizing agents such as carbamoylcholine or KCl were introduced to such a cell in concentrations that normally produce a 20-30 mV depolarization, the abrupt all-or-none depolarization immediately occurred. All-or-none depolarizations arising from either electrical stimulation or depolarizing agents were unaffected by d-tubocurarine but were completely reversed by tetrodotoxin. Batrachotoxin thus appeared to activate only the action potential Na+ channels. In the batrachotoxin-treated membrane, these channels could attain stable steady states in either a closed configuration at the normal resting potential or in an open configuration after complete depolarization. A striking hysteresis cycle thus could be generated, which was strongly indicative of a voltage-dependent interaction of the toxin with the action potential Na+ channels.