Fipronil is a member of the relatively new phenylpyrazole insecticide class that is active at the neuro-inhibitory gamma amino butyric acid (GABA)-gated chloride channel/ionopore complex. The toxicity and neurophysiological effects of fipronil and its oxidative sulfone metabolite [5-amino-1-(2,6-dichloro-4trifluoromethylphenyl)-3-cyano-4-trifluoromethylsulfonylpyrazole] were investigated by using an insecticide-susceptible western corn rootworm population. In topical bioassays using adult rootworms, fipronil was toxic at very low doses (LD 50 = 0.07; LD 90 = 0.33 ng/mg). At the LD 90 , pre-treatment with the cytochrome P450 monooxygenase inhibitor piperonyl butoxide led to mild antagonism of fipronil toxicity (LD 90 = 0.42 ng/mg), while the sulfone analog had greater toxicity (LD 90 = 0.22 ng/ mg). In neurophysiological studies of spontaneous electrical activity, adult and larval rootworms were equally affected by fipronil and the sulfone analog at 10 mM (in the presence of 5 mM GABA) in comparison to GABA-treated baselines. Using larval rootworms, insensitivity of the GABA receptor to binding by picrotoxinin or dieldrin (10 mM ) was not apparent in the presence of 5 mM GABA. Further neurophysiological investigation using a range of concentrations (0.625-20.0 mM) on larval rootworms indicated concentration-dependent effects on bursting activity for both fipronil and the sulfone analog; however, subtle differences were observed between these two compounds. Results indicate that both fipronil and its oxidative sulfone metabolite have similar toxicological and neurological effects on rootworms. Arch. Insect Biochem. Physiol. 40:150-156, 1999.