MODIFICATION OF SODIUM-CHANNEL KINETICS BY THE INSECTICIDE TETRAMETHRIN IN CRAYFISH GIANT-AXONS

Abstract

The effects of the pyrethroid insecticide tetramethrin on voltage-dependent Na channels were studied with internally perfused crayfish giant axons. At low concentrations in the order of 10-8-10-9M, tetramethrin increased depolarizing after-potential which triggered repetitive after-discharges. Under voltage clamp conditions, the Na current was markedly prolonged during a step depolarization and a large and prolonged Na tail current appeared upon step repolarization. A population of Na channels having activation and inactivation kinetics identical to those in control axons was observed in the tetramethrin-poisoned axons, indicating that only a fraction of the channels was modified. The modified channels exhibited remarkably slow kinetics, activating with a time course of 100 ms-2 s and inactivating with a time course of 1-5 s depending on the membrane potential. The voltage dependence of the modified channels was shifted in the direction of hyperpolarization by .apprx. 10-20 mV with respect normal Na channels. The large inward Na tail current associated with step repolarization of the membrane decayed with a time course of 20-600 m. A kinetic hypothesis describing the behavior of Na channels in a tetramethrin-poisoned axon was presented and discussed in relation to the behavior of the Na channels modified by other toxins.