Abstract
The primary mode of action of pyrethroids in insects is to interfere with the normal function of voltage-gated sodium channels (VGSC). We have shown that deactivation kinetics were more deeply affected in VGSC from the sensory neurons of the honey bee, Apis mellifera , than from its brain neurons (Kadala et al 2011 Neurotoxicology, 2014 PLoS one) and suggested from studies using the cloned AmNa V 1 sodium channel, that Na V accessory subunits could partly un- derlie this differential sensitivity (Gosselin-Badaroudine et al 2015, Sci Rep). On the other hand, the side effects of neonicotinoids towards non-target organ- isms (including pollinators), has recently focused the attention and led the European Union to restrict the use of three members of this compounds family. This restriction may mechanically lead to an increase in pyrethroids usage (e.g. deltamethrin, cypermethrin, l -cyalothrin, permethrin). Whereas our past work was focused on domestic honey bee VGSC susceptibility, the impact of pyre- throids on wild bee channels remained largely unknown. Here, the effect of veratridine and two pyrethroids are compared on neuronal VGSCs from the honey bee and Bombus terrestris , a common bumble bee. Modeling the sodium channel as a multi-state channel with fast and slow inactivation mechanisms al- lows a more precise analysis of gating kinetics modifications induced by pyre- throids. Together with molecular modeling, these results give some clues to understand how such compounds could selectively target different species.