Christian Spalthoff, Vincent L. Salgado, Mario Theis, Bart R. H. Geurten, Martin C. Göpfert

The selective aphicide flonicamid is known to cause symptoms in aphids that are like those of chordotonal organ TRPV channel modulator insecticides such as pymetrozine, pyrifluquinazon and afidopyropen. Flonicamid is classified by IRAC as a chordotonal organ modulator with an undefined target site. However, while it has been shown not to act on TRPV channels, flonicamid's action on chordotonal organs has not been documented in the literature. Flonicamid causes locusts to extend their hindlegs, indicating an action on the femoral chordotonal organ. In fruit flies it abolishes negative gravitaxis behavior by disrupting transduction and mechanical amplification in antennal chordotonal neurons. While flonicamid itself only weakly affects locust chordotonal organs, its major animal metabolite 4-trifluoromethylnicotinamide (TFNA-AM) potently stimulates both locust and fly chordotonal organs. Like pymetrozine, TFNA-AM rapidly increases Ca2+ in antennal chordotonal neurons in wild-type flies, but not iav1 mutants, yet the effect is non-additive with the TRPV channel agonist. Flonicamid is a pro-insecticide form of TFNA-AM, a potent chordotonal organ modulator. The functional effects of TFNA-AM on chordotonal organs of locusts and flies are indistinguishable from those of the TRPV agonists pymetrozine, pyrifluquinazon and afidopyropen. Since our previous results indicate that TFNA-AM does not act directly on TRPV channels,1 we conclude that it acts upstream in a pathway that leads to TRPV channel activation. This article is protected by copyright. All rights reserved.