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International audience; Nicotinic acetylcholine receptors (nAChRs) are the main target of neonicotinoid insecticides, which are widely used in crop protection against insect pests. Electrophysiological and molecular approaches have demonstrated the presence of several nAChR subtypes with different affinities for neonicotinoid insecticides. However, the precise mode of action of neonicotinoids on insect nAChRs remains to be elucidated. Radioligand binding studies with [3H]-α-bungarotoxin and [3H]-imidacloprid have proved instructive in understanding ligand binding interactions between insect nAChRs and neonicotinoid insecticides. The precise binding site interactions have been established using membranes from whole body and specific tissues. In this review, we discuss findings concerning the number of nAChR binding sites against neonicotinoid insecticides from radioligand binding studies on native tissues. We summarize the data available in the literature and compare the binding properties of the most commonly used neonicotinoid insecticides in several insect species. Finally, we demonstrate that neonicotinoid-nAChR binding sites are also linked to biological samples used and insect species.

Some quinuclidine benzamide compounds have been found to modulate nicotinic acetylcholine receptors in both mammals and insects. In particular, the quaternarization of 3-amino quinuclidine benzamide derivatives with dichloromethane gave charged N-chloromethylated quinuclidine compounds, disclosing an antagonist profile on homomeric α7 nAChRs. Here, we synthesized and studied the toxicological effect of LMA10233, a quinuclidine-borane complex analogue, the LMA10233, on the pea aphid Acyrthosiphon pisum and found that LMA10233 only exhibit proper toxicity on A. pisum larvae when applied in concentrations of over 10 μg/ml. We assessed the ability of LMA10233 to enhance the toxicity of different insecticides. When a sublethal concentration of LMA10233 was combined with the LC10 of each compound, we found a strong increase in toxicity at 24 h and 48 h of exposure for clothianidin, fipronil and chlorpyrifos, and only at 24 h for imidacloprid, acetamiprid and deltamethrin. However, when the pesticide was used at the LC50, only acetamiprid showed a synergistic effect with LMA10233. When the concentration of LMA10233 was decreased, we found that up to 80–90% of mortality was obtained due to the synergism between acetamiprid and LMA10233. No similar effect was observed with other insecticides. We conclude that such quinuclidine-borane complex compounds could increase the toxic effect of insecticides at low concentrations.

International audience; The intracellular toxicity of the neonicotinoid insecticides imidacloprid and clothianidin was studied on cockroach Periplaneta americana Kenyon cells using the trypan blue exclusion test and the adenylate kinase (AK) detection reagent. To evaluate cytotoxicity, Kenyon cells were exposed to different concentrations (1, 5, 10, 50 and 100 μM) of both imidacloprid and clothianidin at different delays (1, 3, 5, 8 and 24 h). Our data show that both imidacloprid and clothianidin decreased cell viability, with a more pronounced effect following imidacloprid exposure. Indeed, a significant decrease of cell viability was observed for 50 and 100 μM imidacloprid at 8 and 24 h, with trypan blue exclusion test. Study of the AK activity revealed that 50 and 100 μM imidacloprid induced an increase of AK activity, except for 50 μM at 24 h whereas at the same concentrations, clothianidin induced a transient effect at 5 and 8 h. According to previous studies showing that imidacloprid was a partial agonist and clothianidin a full agonist of insect nicotinic acetylcholine receptors, we demonstrated that both imidacloprid and clothianidin were also able to induce distinct intracellular toxic effects