Site-Insensitive Mechanisms in Knockdown-Resistant Strains of House Fly Larva, <i>Musca domestica</i>

Osborne, Michael P.; Pepper, David R.; Hein, Paul; Clark, J. Marshall

doi:10.1021/bk-1995-0591.ch008

Cited by 4 publications

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“…Deltamethrin has previously been shown to modify phosphorylation cascades in the presynaptic nerve terminal of invertebrates Miyazawa and Matsumura 1990;Osborne et al 1995) and vertebrates (Ishikawa et al 1989;Matsumura 1991, 1993;Kanemoto et al 1992). Specifically, deltamethrin was found to stimulate the PKC/phosphoinositide pathway in rat brain synaptosomes, which increased intracellular 1,4,5-triphosphate (IP 3 ) and free Ca 2+ (Enan and Matsumura 1993).…”

Section: Rat Brain Ca V 22 As a Site Of Action For Deltamethrinmentioning

confidence: 99%

Pyrethroid action on calcium channels: neurotoxicological implications

Clark¹,

Symington

2007

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Actions of cismethrin versus deltamethrin were compared using two functional attributes of rat brain synaptosomes. Both pyrethroids increased calcium influx but only deltamethrin increased Ca(2+)-dependent neurotransmitter release following K(+)-stimulated depolarization. The action of deltamethrin was stereospecific, concentration-dependent, and blocked by omega-conotoxin GVIA. These findings delineate a separate action for deltamethrin and implicate N-type rat brain Ca(v)2.2 voltage-sensitive calcium channels (VSCC) as target sites that are consistent with the in vivo release of neurotransmitter caused by deltamethrin. Deltamethrin (10(-7) M) reduced the peak current (approx. -47%) of heterologously expressed wild type Ca(v)2.2 in a stereospecific manner. Mutation of threonine 422 to glutamic acid (T422E) in the alpha(1)-subunit results in a channel that functions as if it were permanently phosphorylated. Deltamethrin now increased peak current (approx. +49%) of T422E Ca(v)2.2 in a stereospecific manner. Collectively, these results substantiate that Ca(v)2.2 is directly modified by deltamethrin but the resulting perturbation is dependent upon the phosphorylation state of Ca(v)2.2. Our findings may provide a partial explanation for the different toxic syndromes produced by these structurally-distinct pyrethroids.

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Section: Rat Brain Ca V 22 As a Site Of Action For Deltamethrinmentioning

confidence: 99%

Pyrethroid action on calcium channels: neurotoxicological implications

Clark¹,

Symington

2007

Invert Neurosci

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“…Evidence of mechanisms of deltamethrin resistance in other studies suggests that this is speciesspecific. The housefl!, Musca domestica,exhibits mechanisms involving siteinsensitivity (Osborne et al 1995) while other species such as p. rylostellahave esterases that play an important role (Kim er al. 1996).…”

Section: Discussionmentioning

confidence: 99%

Aspects of Insecticide Resistance in New Zealand Strains of the Sheep Blowflies, Lucilia Cuprina and Lucilia Sericata

Wilson¹

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<p>A treated surface bioassay was used to detect insecticide resistance to five organophosphorus insecticides (diazinon, chlorfevinphos, chlorpyrifos, dichlofenthion and propetamphos), the synthetic pyrethroid, deltamethrin, and the insect growth regulator, diflubenzuron, in larvae of field strains of Lucilia cuprina, and diazinon in Lucilia sericata from 1990 to 1997. Organophosphate resistance was widespread in both species of blowfly and L. cuprina exhibited side-resistance between diazinon, chlorpyrifos, dichlofenthion and propetamphos but no cross-resistance could be demonstrated with diazinon and deltamethrin, or between diazinon and diflubenzuron. Phenotypic expression of resistance appeared to be influenced by environmental factors such as season, region, sheep density and year. The relative efficacies of four of the above OPs and the extent to which the OP resistance status of L. cuprina affected this, was assessed by comparing a susceptible strain of L. cuprina, and a strain known to exhibit OP side-resistance, in a series of in vivo trials. All four treatments provided 19 - 21 weeks protection against susceptible larvae but chlorfenvinphos provided the longest protection (16 - 17 weeks), followed by propetamphos (15 - 16 weeks), dichlofenthion (10 - 13 weeks) and diazinon (9 - 13 weeks), against the resistant strain. Penetration of insect cuticle, non-oxidative and oxidative mechanisms that might contribute to resistance to organophosphate insecticides were examined in larvae and adults from field isolates of L. cuprina. Only non-oxidative mechanisms were considered with respect to L. sericata. The basal mechanism of resistance appeared to be an altered esterase (the E3 esterase) in L. cuprina and was also suspected to contribute to OP-resistance in L. sericata. Adult and larval strains of L. sericata showed no relationship between level of GST conjugating activity and resistance to diazinon, suggesting that these enzymes do not constitute a mechanism of OP-resistance in this species. Contrasting this was the observation of a strong relationship between the level of GST conjugating activity, with respect to model substrate DCNB, and resistance to diazinon in both adult and larval strains of L. cuprina. This relationship was supported by a study of the OP-conjugating properties of partially purified glutathione S-transferases from resistant L. cuprina larvae. Neither an increase in acetylcholinesterase content nor an insensitive AChE in the central nervous system of larvae of L. cuprina and larvae or adult L. sericata appear to have been selected for in the resistant field strains examined. There did however appear to be a positive correlation between resistance to diazinon and susceptibility of AChE inactivation by tetrachlorvinphos in L. cuprina adults. The significance of this factor was investigated further by multiple regression and it was concluded that this did not have a main effect on resistance in adults. Samples of L. cuprina were further characterised by RAPD-PCR to determine intra-and inter-strain variation. Key features of this analysis were the calculation of phylogenetic similarities in an attempt to better define a 'field strain', the mode of dispersal of the species throughout New Zealand as well as to identify genetic markers of high level insecticide resistance. No markers of resistance were identified but this study emphasised the need to treat each sample as a separate strain as sampling from the same area at different times showed that samples were not identical suggesting there is variable gene flow in and out of areas and populations. Based on biochemical identification of resistance mechanisms, consideration was given to the use of potentiating pairs of insecticides as a method of prolonging the life of some existing OP insecticides. It was shown that prospects for using such pairs is limited due to the widespread OP-resistance observed in L. cuprina. Finally, rather than reiterate discussion of resistance mechanisms, the conclusion of this thesis looks towards applying knowledge of resistance mechanisms effectively within the framework of integrated pest management system (IPM). It discusses areas of weakness in knowledge that need to be addressed and emphasises the need for a susceptibility reservoir if IPM is to succeed at a national level.</p>

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Identification of mutations in the houseflypara-type sodium channel gene associated with knockdown resistance (kdr) to pyrethroid insecticides

et al. 1996

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We report the isolation of cDNA clones containing the full 6.3-kb coding sequence of the para-type sodium channel gene of the housefly, Musca domestica. This gene has been implicated as the site of knockdown resistance (kdr), an important resistance mechanism that confers nerve insensitivity to DDT and pyrethroid insecticides. The cDNAs predict a polypeptide of 2108 amino acids with close sequence homology (92% identity) to the Drosophila para sodium channel, and around 50% homology to vertebrate sodium channels, Only one major splice form of the housefly sodium channel was detected, in contrast to the Drosophila para transcript which has been reported to undergo extensive alternative splicing. Comparative sequence analysis of housefly strains carrying kdr or the more potent super-kdr factor revealed two amino acid mutations that correlate with these resistance phenotypes. Both mutations are located in domain II of the sodium channel. A leucine to phenylalanine replacement in the hydro-phobic IIS6 transmembrane segment was found in two independent kdr strains and six super-kdr strains of diverse geographic origin, while an additional methionine to threonine replacement within the intracellular IIS4-S5 loop was found only in the super-kdr strains. Neither mutation was present in five pyrethroid-sensitive strains. The mutations suggest a binding site for pyrethroids at the intracellular mouth of the channel pore in a region known to be important for channel inactivation.

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Site-Insensitive Mechanisms in Knockdown-Resistant Strains of House Fly Larva, Musca domestica

Cited by 4 publications

References 0 publications

Pyrethroid action on calcium channels: neurotoxicological implications

Pyrethroid action on calcium channels: neurotoxicological implications

Aspects of Insecticide Resistance in New Zealand Strains of the Sheep Blowflies, Lucilia Cuprina and Lucilia Sericata

Identification of mutations in the houseflypara-type sodium channel gene associated with knockdown resistance (kdr) to pyrethroid insecticides

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