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Metaflumizone inhibits the honeybee Na V 1 channel by targeting recovery from slow inactivation
Author(s) -
GosselinBadaroudine Pascal,
Charnet Pierre,
Collet Claude,
Chahine Mohamed
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12897
Subject(s) - xenopus , chemistry , channel (broadcasting) , kinetics , biophysics , pharmacology , toxicology , biology , biochemistry , computer science , physics , computer network , gene , quantum mechanics
Metaflumizone is the latest addition to the armamentarium of the Na + channel inhibitor insecticide family. We used the Xenopus oocyte expression system and a Markovian model to assess the effect of metaflumizone on Apis mellifera Na + channels (AmNa V 1). Our results reveal that metaflumizone inhibits AmNa V 1 channels by targeting the kinetics of recovery from slow inactivation. Multistate modeling of fast and slow inactivation of the AmNa V 1 channel made it possible to study the effects of metaflumizone on a set of rate constants underlying the transition between the open and inactivated conformations and provided insights into their specificity. We conclude that the methods we used could be extended to assessing the toxicity of other Na + channel inhibitor insecticides.