The insecticide imidacloprid is a partial agonist of the nicotinic receptor of honeybee Kenyon cells

An update of the Worldwide Integrated Assessment (WIA) on systemic insecticides. Part 1: new molecules, metabolism, fate, and transport

“…Taylor-Wells et al (2015) found that a potential secondary target of imidacloprid is the GABA receptor Rdl in Anopheles gambiae, where imidacloprid acts as an antagonist. Their conclusion is consistent with previous observations that imidacloprid lessens GABA-induced responses in cultured honeybee (Apis mellifera) Kenyon cells (Deglise et al 2002;Taylor-Wells et al 2015). In addition, imidacloprid decreases the density of the synaptic units in the region of the calyces of mushroom bodies in honeybee brain (Peng and Yang 2016).…”

Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death

“…Empirical evidence demonstrates that desensitization of nAChRs in honey bee Kenyon cells leads to antagonistic behavior of the receptor, effectively closing the receptor (Deglise et al, 2002) as described in the KE1 section. Closure of the receptor, due to prolonged desensitization is likely to impede Ca 2+ signaling across the nAChR and, hence, downstream components of the pathway, although studies specifically evaluating such desensitization and impacts on Ca 2+ signaling in the insect neuron are lacking.…”

“…Exposure of cultured Kenyon cells from honey bee brains to imidacloprid yielded partial nAChR agonist activity, eliciting 36% of the ACh-induced current and causing desensitization of the receptor after prolonged (16 s) exposure (Deglise et al, 2002). Further, when 10 − 5 M imidacloprid was co-applied with ACh, the mean amplitude of ACh-induced currents was significantly lowered (64%) compared to ACh coapplication with saline, thereby providing evidence that imidacloprid antagonized the ACh-induced receptor activation by out-competing ACh for the same binding site (Deglise et al, 2002).…”

“…Exposure of cultured Kenyon cells from honey bee brains to imidacloprid yielded partial nAChR agonist activity, eliciting 36% of the ACh-induced current and causing desensitization of the receptor after prolonged (16 s) exposure (Deglise et al, 2002). Further, when 10 − 5 M imidacloprid was co-applied with ACh, the mean amplitude of ACh-induced currents was significantly lowered (64%) compared to ACh coapplication with saline, thereby providing evidence that imidacloprid antagonized the ACh-induced receptor activation by out-competing ACh for the same binding site (Deglise et al, 2002). Interestingly, an antagonist of the nAChR (mecamylamine) demonstrated similar properties, likely affecting neurotransmission, in that direct injection into the brain hemolymph of honey bee was shown to not only impair olfactory learning but, in patch-clamp experiments with cultured Kenyon cells, completely block the ACh-induced current (Lozano et al, 1996;Wüstenberg and Grünewald, 2004).…”

“…The primary location of insect nAChRs is the brain. In honey bees, nAChRs have been identified in Kenyon cells located on mushroom bodies and antennal lobes, both involved in olfactory learning (Deglise et al, 2002;Dupuis et al, 2011).…”