TOXICOLOGICAL, ELECTROPHYSIOLOGICAL, AND MOLECULAR CHARACTERIZATION 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 r esistance in a Taiwanese strain of the diamondback moth, Plutella xylo stella. Initial evidence for this type of target site insensitivity, a lso termed knockdown resistance or kdr, was provided by nonsynergizabl e cross-resistance to a range of pyre throids and DDT and an incomplet ely recessive autosomal inheritance of the resistance trait. This was corroborated by using a larval neuromuscular preparation to assess spo ntaneous miniature excitatory postsynaptic potentials (mEPSPs) and evo ked EPSPs in response to varying concentrations of the pyrethroid delt amethrin. Intracellular recordings revealed a pyrethroid-induced incre ase in mEPSP activity and a decline in the EPSP amplitude; responses w ere induced only at considerably higher concentrations in resistant la rvae when compared to larvae of a susceptible standard strain. These f indings were supported by the detection of two amino acid changes in p art of the pam-type voltage-sensitive sodium channel (the primary targ et site of pyrethroids) of the resistant strain. One of these mutation s, a leucine to phenylalanine replacement in transmembrane segment 6 o f domain II, has previously been shown to correlate with kdr in the ho use fly, Musca domestica, and German cockroach, Blattella germanica. ( C) 1998 Academic Press.