Abstract

The pyrethroid insectide decamethrin (10 −6M) caused a frequency-dependent depression of the action potential in frog myelinated nerve fibres which was associated with a progressive membrane depolarisation brought about by summation of depolarising after-potentials. Voltage clamp experiments with single nodes of Ranvier showed that this afterpotential was most probably due to a long-lasting prolongation of the transient increase in sodium permeability of the membrane. The results indicate that decamethrin, like the other pyrethroids, specifically affects the sodium channels of the nerve membrane.

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