Toxicological, electrophysiological, and molecular characterisation of knockdown resistance to pyrethroid insecticides in the diamondback moth, Plutella xylostella (L.)

Nerve insensitivity was shown to be a major cause of high pyrethroid resistance in a Taiwanese strain of the diamondback moth, Plutella xylostella. Initial evidence for this type of target site insensitivity, also termed knockdown resistance or kdr, was provided by nonsynergizable cross-resistance to a range of pyre throids and DDT and an incompletely recessive autosomal inheritance of the resistance trait. This was corroborated by using a larval neuromuscular preparation to assess spontaneous miniature excitatory postsynaptic potentials (mEPSPs) and evoked EPSPs in response to varying concentrations of the pyrethroid deltamethrin. Intracellular recordings revealed a pyrethroid-induced increase in mEPSP activity and a decline in the EPSP amplitude; responses were induced only at considerably higher concentrations in resistant larvae when compared to larvae of a susceptible standard strain. These findings were supported by the detection of two amino acid changes in part of the pam-type voltage-sensitive sodium channel (the primary target site of pyrethroids) of the resistant strain. One of these mutations, a leucine to phenylalanine replacement in transmembrane segment 6 of domain II, has previously been shown to correlate with kdr in the house fly, Musca domestica, and German cockroach, Blattella germanica. (C) 1998 Academic Press.