Toxicity and neurophysiological effects of selected insecticides on the mole cricket, Scapteriscus vicinus (Orthoptera: Gryllotalpidae)

Mole crickets (Scapteriscus spp.) are severe subterranean pests of turfgrasses, commonly targeted with neurotoxic insecticides. Ideally insecticides used against mole crickets should induce quick knockdown or mortality to minimize damage caused by their tunneling. However, neurophysiological effects of insecticides on mole crickets are mostly unknown. The aims of this study were to investigate neurophysiological and toxic effects of several insecticides on tawny mole cricket (Scapteriscus vicinus Scudder) adults and nymphs, and potential synergy between pyrethroid and neonicotinoid insecticides. Bifenthrin, fipronil, and the combination of bifenthrin + imidacloprid provided the fastest median mortality when injected. The combination of bifenthrin + imidacloprid elicited faster toxicity than either active ingredient alone. Imidacloprid, bifenthrin, and bifenthrin + imidacloprid caused immediate knockdown, whereas fipronil immobilized mole crickets within 1-2 h. Acephate, bifenthrin, fipronil, imidacloprid, and bifenthrin + imidacloprid caused significant neuroexcitation. Bifenthrin + imidacloprid resulted in greater increases of spontaneous neural activity than the additive effects of imidacloprid and bifenthrin alone. Excitatory compounds acting at sodium and chloride channels (bifenthrin and fipronil) were the most toxic against S. vicinus. Combining a sodium channel toxin (bifenthrin) and a synaptic toxin (imidacloprid) led to greater than additive neurophysiological and toxic effects, which to our knowledge provides the first documented evidence of synergistic neurological “potentiation”.