Two insect Transient Receptor Potential (TRP) channel proteins, Nanchung (Nan) and Inactive (Iav), form a heteromeric TRP-vanilloid (TRPV) channel that is expressed exclusively in chordotonal stretch receptor neurons and is essential for mechanosensory function. Activation of the TRPV channel by the pyridine azomethine derivative insecticides pymetrozine and pyrifluquinazon (Neuron, 86:665-671, 2015) and the novel pyropene insecticide afidopyropen (Insect Biochem. Molec. Biol. 84:32-39, 2017) disrupts the senses of proprioception, kinesthesia, hearing, gravity, balance, and acceleration. Without these senses, affected insects are uncoordinated and disoriented; sucking pests in this state cannot feed and starve to death. The endogenous mechanism of activation of TRPV channels by mechanical stimuli has not yet been determined, but it was recently shown that nicotinamide (NAM) is an endogenous activator of TRPV channels in the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. (Nature Commun. 7: 13135, 2016) Here we report that exogenous NAM increases the firing rate of the cockroach cercal chordotonal organ and that inhibition of NAM degradation by the nicotinamidase inhibitor nicotinaldehyde increases the basal firing rate slightly and increases the sensitivity to exogenous NAM by 100-fold, indicating that chordotonal organ firing is regulated by endogenous NAM. We also investigated the activation of pea aphid Nan-Iav heteromers expressed in Xenopus oocytes. Elevated extracellular Ca2+ concentration or exogenous NAM activated the channels, while single channels in excised patches were activated by NAM but not Ca2+, indicating that NAM but not Ca2+ directly activates the channels. In summary, we have shown that nicotinamide is an endogenous regulator of chordotonal organ activity that directly activates TRPV channels.

Nicotinamide is an endogenous modulator of insect chordotonal organs

2019 Fall National Meeting

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