Flupyradifurone, imidacloprid and clothianidin disrupt the auditory processing in the locust CNS.

Abstract

Since the EU banned classic neonicotinoids like imidacloprid and clothianidin, they may be replaced by more recently marketed insecticides such as flupyradifurone. However, they all operate on the same neuropharmacological principle as selective agonists at the insect's nicotinic acetylcholine receptors. Here we investigated the impact of flupyradifurone, imidacloprid and clothianidin on the neuronal processing in the auditory pathway of the desert locust Schistocerca gregaria. While stepwise increasing the insecticide concentration in the haemolymph, we extracellularly recorded the spike responses of auditory afferents in the tympanal nerve and of auditory interneurons in the neck connectives. All three insecticides showed a very similar dose-dependent suppression of spike responses in the auditory interneurons ascending towards the brain, whereas the spike responses in the sensory neurons of the ears appeared unaffected. Furthermore, by systematic injection experiments we demonstrate that insecticide dosages which already supress the information transfer in the auditory pathway are by far too low to induce the typical poisoning symptoms like trembling, spasms, and paralysis. We discuss how sublethal intoxication with classical neonicotinoids or functionally related insecticides like flupyradifurone may disrupt the postsynaptic balance between excitation and inhibition in the auditory pathway of locusts and other orthopteran insects.