Effects of Goniopora toxin on crayfish giant axons

The effects of Goniopora toxin (GPT), isolated from the coral Goniopora species, on the crayfish giant axon have been studied by means of microelectrode and sucrose-gap voltage clamp techniques. When applied externally at a concentration of 0.1 microM or higher, the falling phase of the action potential was prolonged markedly. At concentrations over 0.3 microM, GPT gradually depolarized the membrane to 0 mV. The depolarization was not reversed by 1 microM tetrodotoxin or low-Na (1 mM) solution. The amplitude of action potential was slowly decreased in a manner dependent upon the concentration even in the absence of membrane depolarization. Voltage clamp experiments with internally perfused axons have revealed that the falling phase of the sodium current is prolonged markedly and is expressed by two exponential functions. The peak amplitude was first increased and then slowly decreased, and the tail sodium current associated with a step repolarization was slowed. The reversal potential for peak current was not changed by GPT, and the steady-state sodium inactivation was not shifted along the voltage axis. Leakage current gradually increased in the course of GPT action, while the steady-state potassium current was not affected. These effects of GPT were exerted only when it was applied externally and not reversed by washing with toxin-free medium. It is concluded that GPT modifies a fraction of sodium channels to give rise to a prolonged sodium current which is responsible for the prolongation of action potential.