Cellular and molecular mechanisms of action of insecticides: neurophysiological approach

Abstract

The symptoms of poisoning caused by pyrethroids are characterized by ataxia, loss of coordination, hyperexcitation, convulsions, and paralysis. Depending on the type of pyrethroid, repetitive discharges and/or conduction block are observed in various regions of the nervous system. Type I pyrethroids as represented by allethrin and tetramethrin which lack a cyano group cause repetitive discharges in nerve fibers and nerve terminals leading to hyperexcitation of the animal. Type II pyrethroids as represented by cyphenothrin, deltamethrin and fenvalerate which contain a cyano group at the alpha-carbon cause nerve membrane depolarization and block leading to paralysis of the animal. Both types of action are ascribed to modifications of nerve membrane sodium channels which result in very slow gating kinetics. Patch clamp single channel recording experiments have clearly demonstrated that individual sodium channels are modified by tetramethrin in an all-or-none manner to give rise to a prolonged opening without change in conductance. Thus, it is concluded that the site of action of pyrethroids is the sodium channel, and that pyrethroids interact with the channel macromolecules that control the gating mechanism.