Superparasitism by a parasitoid wasp: The absence of sublethal effects from the neonicotinoid insecticide imidacloprid enlightens the specificity of the cholinergic pathway involved.

Imidacloprid is an insecticide that is used globally and is suspected to be at least partly responsible for the decrease in the number of pollinator insects. The effects of an LC20 of imidacloprid on the parasitic behavior of the parasitoid wasp Leptopilina boulardi were investigated. Two genetically identical L. boulardi strains were used for the experiments. The strains differed in that one was infected by LbFvirus and the other was not. LbFvirus is a virus that induces an increase in the superparasitism behavior of the wasp. Results of two previous works have shown that the organophosphorus insecticide chlorpyrifos induces an increase in the superparasitism rate of L. boulardi through its specific action on cholinergic nervous pathways. Imidacloprid targets receptors implicated in cholinergic nervous pathways and thus it was expected that imidacloprid would also increase the superparasitism rate of L. boulardi. However, the results of the present experiment demonstrate that imidacloprid does not interfere with the parasitic behavior of L. boulardi and does not increase the rate of superparasitization. It can then be concluded that the major target of imidacloprid, namely type 1 α-bungarotoxin resistant nicotinic acetylcholine receptors (nAChR1), which imidacloprid is an agonist of, and the minor target, type D α-bungarotoxin sensitive nicotinic acetylcholine receptors (nAChRD), which imidacloprid is an antagonist of, are not involved in the superparasitism behavior by L. boulardi. Therefore, the superparasitism behavior of the parasitoid wasp is controlled by cholinergic pathways that do not involve nAChR1 or nAChRD subtype receptors. These findings may enable a better understanding of the mechanisms by which the LbFvirus acts, and contribute to a better evaluation of the potential environmental impact of imidacloprid use.