CHARACTERIZATION OF BATRACHOTOXIN-INDUCED DEPOLARIZATION OF THE SQUID GIANT AXONS

¹ Department of Pharmacology, Schools of Medicine and Dentistry, State University of New York at Buffalo, Buffalo, New York and Department of Physiology and Pharmacology, Duke University Medical Center, Durham, North Carolina

Characteristics of the depolarizing action of batrachotoxin (BTX) on squid giant axons have been studied in the presence of lithium ions, tetrodotoxin (TTX) and local anesthetics. Substitution of lithium for sodium in the bathing medium did not alter the responsiveness of the axon membrane to BTX; the membrane was depolarized by BTX and repolarized by TTX and 1 mM Li⁺. The minimum concentration of BTX capable of depolarizing the axon membrane was estimated to be less than 10 nM, and the concentration of TTX required to restore the BTX-induced membrane depolarization by 50% was 20 nM. Procaine (0.1-10 mM), applied during the course of the decrease in membrane potential produced by BTX, halted the progressive depolarization. No depolarization occurred during or after simultaneous application of procaine and BTX. Lidocaine and QX-572 did not affect the membrane depolarization produced by BTX. It is suggested that procaine prevents the binding of BTX to the receptor in the axon membrane.

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