Supersensitivity to tetrodotoxin and lidocaine of anthopleurin-A-treated Na+ channels in crayfish giant axon.

Anthopleurin-A produced two distinct responses in crayfish giant axons: depolarization and prolongation of action potentials. The depolarization was prominent at low concentrations of anthopleurin-A, while a remarkable prolongation of the action potential was produced by higher concentrations of anthopleurin-A. Both effects of anthopleurin-A were inhibited by pre- or posttreatment with tetrodotoxin or lidocaine at concentrations which had not effect on the normal sodium channel. The prolongation of the action potential was more sensitive to tetrodotoxin and lidocaine than the depolarization was. These results suggest that sodium channels of the crayfish giant axon are modified by anthopleurin-A in at least two ways, thereby resulting in sensitization to tetrodotoxin and lidocaine.