Comparative analysis of neonicotinoid binding to insect membranes: II. An unusual high affinity site for [3H]thiamethoxam in Myzus persicae and Aphis craccivora

Neonicotinoids represent a class of insect-selective ligands of nicotinic acetylcholine receptors. Imidacloprid, the first commercially used neonicotinoid insecticide, has been studied on neuronal preparations from many insects to date. Here we report first intrinsic binding data of thiamethoxam, using membranes from Myzus persicae Sulzer and Aphis craccivora Koch. In both aphids, specific binding of [3H]thiamethoxam was sensitive to temperature, while the absolute level of non-specific binding was not affected. In M persicae, binding capacity (Bmax) for [3H]thiamethoxam was ca 450 fmol mg(-1) of protein at 22 degrees C and ca 700 fmol mg(-1) of protein at 2 degrees C. The negative effect of increased temperature was reversible and hence not due to some destructive process. The affinity for [3H]thiamethoxam was less affected by temperature: Kd was ca 11 nM at 2 degrees C and ca 15 nM at 22 degrees C. The membranes also lost binding sites for [3H]thiamethoxam during prolonged storage at room temperature, and upon freezing and thawing. In A craccivora, [3H]thiamethoxam was bound with a capacity of ca 1000 fmol mg(-1) protein and an affinity of ca 90 nM, as measured at 2 degrees C. Overall, the in vitro temperature sensitivity of [3H]thiamethoxam binding was in obvious contrast to the behaviour of [3H]imidacloprid studied in parallel. Moreover, the binding of [3H]thiamethoxam was inhibited by imidacloprid in a non-competitive mode, as shown with M persicae. In our view, these differences demonstrate that thiamethoxam and imidacloprid, which represent different structural sub-classes of neonicotinoids, do not share the same binding site or mode. This holds also for other neonicotinoids, as we report in a companion article.     

Efficacy of plant metabolites of imidacloprid against Myzus persicae and Aphis gossypii (Homoptera: Aphididae)

The metabolism of the chloronicotinyl insecticide imidacloprid is strongly influenced by the method of application. Whilst in foliar application most of the residues on the leaf surface display unchanged parent compound, most of the imidacloprid administered to plants by soil application or seed treatment is metabolized more or less completely, depending on plant species and time. The present study revealed that certain metabolites of imidacloprid which have been described in crop plants are highly active against aphid pests in different types of bioassays. Some of these metabolites showed a high oral activity against the green peach aphid (Myzus persicae), and the cotton aphid (Aphis gossypii). The aphicidal potency of the metabolites investigated was weaker in aphid dip tests than in oral ingestion bioassays using artificial double membranes. The most active plant metabolite was the imidazoline derivative of imidacloprid. The LC₅₀ values of this metabolite for M. persicae and A. gossypii in oral ingestion bioassays were in the lower ppb-range, i.e. 0·0044 and 0·0068 mg litre^-1, respectively. Most of the other reported metabolites showed much weaker activity. Compared to imidacloprid, the imidazoline derivative showed superior affinity to housefly (Musca domestica) head nicotinic acetylcholine receptors, while all other metabolites were less specific than imidacloprid. It seems possible that, after seed treatment or soil application, a few of the biologically active metabolites arising are acting in concert with remaining levels of the parent compound imidacloprid, thus providing good control and long-lasting residual activity against plant-sucking pests in certain crops. © 1998 SCI.     

Antifeedant effect,biological efficacy and high affinity binding of imidacloprid to acetylcholine receptors in Myzus persicae and Myzus nicotianae

It is known from laboratory studies that tobacco-associated forms of Myzus persicae (Sulzer) and the closely related tobacco aphid Myzus nicotianae (Blackman) are often somewhat less susceptible to imidacloprid than non-tobacco strains of M. persicae. Choice tests (floating leaf technique) showed that tobacco aphids were also less susceptible to the antifeedant potential of imidacloprid in contact bioassays. Synergists like piperonyl butoxide or DEF did not enhance the susceptibility of tobacco-associated morphs of Myzus ssp. to imidacloprid, thus providing evidence that neither oxidative detoxication nor hydrolytic metabolization took place. However, in an attempt to study the influence of endosymbiotic bacteria on the efficacy of imidacloprid, we allowed small populations of tobacco aphids to feed on diets containing the antibiotic chlortetracycline prior to imidacloprid treatment. While the effectiveness of imidacloprid, i.e. lower LC₅₀ values, could be improved in all strains, including the susceptible reference strain, there was no change in overall tolerance factors. In order to investigate any possible alteration of the target site, the affinity of imidacloprid and nicotine to nicotinic acetylcholine receptors in whole-aphid homogenates was measured. All strains (and clones) showed the same high-affinity binding sites and no detectable difference. Studies using the FAO dip method revealed that the lower susceptibility of M. nicotianae is not restricted to chloronicotinyls like imidacloprid or acetamiprid, because other insecticides with different modes of action such as pymetrozine and fipronil were also affected in laboratory studies. It is considered that the observed tolerance to chloronicotinyls in certain strains of Myzus ssp. is a natural variation in response, probably not coupled with any known mechanism of resistance in this species complex. © 1998 SCI     

Correlated responses to neonicotinoid insecticides in clones of the peach-potato aphid, Myzus persicae (Hemiptera: Aphididae)

BACKGROUND: Although there are still no confirmed reports of strong resistance to neonicotinoid insecticides in aphids, the peach-potato aphid (Myzus persicae Sulzer) shows variation in response, with some clones exhibiting up to tenfold resistance to imidacloprid. Five clones varying in response to imidacloprid were tested with four other neonicotinoid molecules to investigate the extent of cross-resistance.RESULTS: All four compounds-thiamethoxam, thiacloprid, clothianidin and dinotefuran-were cross-resisted, with ED(50) values ranked in the same order as for imidacloprid. Resistance factors ranged up to 11 for imidacloprid, 18 for thiamethoxam, 13 for thiacloprid, 100 for clothianidin and 6 for dinotefuran.CONCLUSION: This variation in response does not appear to be sufficient to compromise the field performance of neonicotinoids aimed at controlling aphids. However, it highlights the need for careful vigilance and stewardship in all M. persicae populations, and a need to consider neonicotinoids as a single cross-resisted group for management purposes.     

Green peach aphid,Myzus persicae (Hemiptera: Aphididae), reproduction during exposure to sublethal concentrations of imidacloprid and azadirachtin

BACKGROUND: Resurgence of insect pests following insecticide applications is often attributed to natural enemy disturbance, but hormesis could be an alternative or additional mechanism. Green peach aphid, Myzus persicae (Sulzer), is an important insect pest of many crops worldwide that may be exposed to sublethal insecticide concentrations over time. Here, the hypothesis that exposure to low concentrations of imidacloprid and azadirachtin can induce hormetic responses in M. persicae is tested in the laboratory. RESULTS: When insects were exposed to potato leaf discs dipped in sublethal concentrations of insecticide, almost all measured endpoints—adult longevity, F1 production, F1 survival and F2 production—were affected, and a statistically significant (P < 0.05) stimulatory response was recorded for F2 production following exposure to imidacloprid. No other measures for hormesis were statistically significant, but other trends of hormetic response were consistently observed. CONCLUSIONS: Given that variable distribution and degradation of insecticides in the field would result in a wide range of concentrations over time and space, these laboratory experiments suggest that exposure to sublethal concentrations of imidacloprid and azadirachtin could stimulate reproduction in M. persicae. Copyright © 2008 Society of Chemical Industry     

Susceptibility of standard clones and European field populations of the green peach aphid, Myzus persicae, and the cotton aphid, Aphis gossypii (Hemiptera: Aphididae), to the novel anthranilic diamide insecticide cyantraniliprole

BACKGROUND: Parthenogenetic clones of the green peach aphid, Myzus persicae (Sulzer), and the cotton aphid, Aphis gossypii Glover, were tested with the anthranilic diamide insecticide cyantraniliprole (i.e. DuPont^? Cyazypyr^?) in systemic‐uptake bioassays to investigate potential for cross‐resistance conferred by mechanisms of insecticide resistance to organophosphates, carbamates and pyrethroids and, in the case of M. persicae, reduced sensitivity to neonicotinoids. These data were compared with the response of field samples of M. persicae and A. gossypii collected from around Europe. RESULTS: Cyantraniliprole was not cross‐resisted by any of the known insecticide resistance mechanisms present in M. persicae or A. gossypii. The compound was equally active against resistant and susceptible aphid strains. The responses of the M. persicae field samples were very consistent with a maximum response ratio of 2.9 compared with a standard laboratory clone. The responses of the A. gossypii field samples were more variable, although a majority of the responses were not statistically different. CONCLUSION: Cyantraniliprole is currently the only anthranilic diamide (IRAC MoA 28) insecticide targeting aphid species such as M. persicae and A. gossypii. There is no evidence to suggest that the performance of this compound is affected by commonly occurring mechanisms that confer resistance to other insecticide chemistries. Cyantraniliprole is therefore a valuable tool for managing insecticide resistance in these globally important pests. Copyright © 2011 Society of Chemical Industry