Intracellular mechanisms and cellular responses to Ca2+ require intermediary proteins such as calcium/calmodulin-dependent protein kinase II (CaMKII) and cAMP, which transduce the signal into downstream effects. In the present study, we demonstrated that CaMKII and cAMP modified neonicotinoid sensitivity agiants insect nicotinic acetylcholine receptors. CaMKII and cAMP differently affected neonicotinoid responses and thus were involved in insect resistance mechanisms against insecticides. Moreover, we proposed that neonicotinoid efficiency could be altered by specific inhibition of CaMKII or cAMP, resulting that the same nicotinic receptor subtype is differently sensitive to clothianidin and imidaclorpd. We propose that phosphorylation/dephosphorylation process and intracellular pathways involved in the regulation of insect nicotinic acetylcholine receptors could differently affect neonicotinoid efficacy.

Modulation of neonicotinoid toxicity by intracellular pathways regulating insect nicotinic acetylcholine receptor function

248th National Meeting (2014)

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