6533b854fe1ef96bd12afb50

RESEARCH PRODUCT

Pyrethroids alter sodium channel gating in honeybee olfactory receptor neurons

Aklesso KadalaMercedes CharretonIngrid JakobYves Le ConteClaude Collet

subject

[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]honeybeeolfactory receptor neurons[SDV.AEN]Life Sciences [q-bio]/Food and NutritionComputingMilieux_MISCELLANEOUS

description

International audience; Social structure in a domestic honeybee colony relies on inter-individual. chemical communication. Chemical communication is mediated. by odors and pheromones detected by olfactory receptor. neurons (ORN) localized in antennae. The Colony Collapse Disorder. (CCD) has been described in many countries around the world. and one of its main symptoms is the desertion of the hive by adult. worker bees, leaving the queen with brood and a small number of. young bees only. Our hypothesis is that such a desertion could be a. consequence of a disruption in the colony cohesion due to a defective. peripheral olfactory system. Recent studies have shown that. several insecticides can be found inside the hive, including members. of the pyrethroid insecticides familly widely used in agriculture (e.g. in USA, Mullin et al. 2010 PLoS One 5). To study the consequences of an exposure of isolated ORNs to. pyrethroids insecticides, we used electrophysiology. ORNs from. honeybee prepupae were isolated and kept in cell culture according. a procedure described earlier (Laurent et al. 2002 Eur J Neurosci. 15). A disposable gravity driven perfusion system or a multicapillary. system were used to control extracellular solutions composition. and allowed exposure of ORNs to various insecticides and neurotoxins. In appropriate ionic conditions, we characterized under. voltage-clamp the sensitivity of the voltage-dependent sodium current. (INa) to the fish toxin tetrodotoxin (TTX), and to type I and. type II pyrethroids. Our results show that pyrethroids induce a TTX-sensitive tail current. upon repolarization by slowing down the sodium channel closing. On average, after a single 3 ms stimulation, 10 lM permethrin. or tetramethrin modify 20 ± 4 and 22 ± 7% of sodium channels. respectively. Evidence for a higher percentage of modified channels. at these concentrations are given by repetitive stimulations, since. more than 80% channels happen to be modified by a train of 10. pulses at 35 Hz. Similar percentages were obtained in the presence. of some invertebrate toxins. Whereas the sea anemone toxin ATXII. slowed inactivation by a factor 150, the scorpion toxin AaHII had. no effect at a concentration of 20 nM. Interestingly, ATX-II. increased the maximal current peak amplitude by a factor 1.5,. which suggests that a large fraction of channels inactivate without. opening at Vmax. ATX-II has no effect on current deactivation. In. the presence ATX-II, a single 3 ms pulse give a maximal tail current. amplitude and a fraction of modified channels close to 80%, a result. that challenges the hypothesis of a use-dependent effect. The pyrethroid-. induced modification of sodium channels involved in action. potential could be responsible for abnormal information processing. in antennal olfactory receptor neurons and would lead to defective. detection of odors and pheromones if pyrethroids reach sufficient. concentrations in vivo.

https://hal.inrae.fr/hal-02643384