Abstract The phenylpyrazole insecticide fipronil is the first compound of its class to be registered for commercial use. The mode of action of this class of insecticides involves antagonism of the inhibitory neurotransmitter, γ-aminobutyric acid (GABA). The sulfone metabolite of fipronil has been reported to be similar in toxicity to the parent compound. In this study, the toxicity and neurophysiological effects of fipronil and the sulfone metabolite were determined for European corn borer larvae. Fipronil was very toxic to neonate European corn borer larvae in feeding bioassays (LC50 = 3.34 ng a.i./cm2 of treated diet) and to fifth instars in topical bioassays (LD50 = 18.78 ng/insect). The sulfone metabolite was slightly more toxic to neonate larvae (LC50 = 1.44 ng a.i./cm2) and equally toxic to fifth instar larvae (LD50 = 19.54 ng/insect) compared with the parent compound. Neonate larvae preexposed to piperonyl butoxide (PBO) residues coated on the inside of glass scintillation vials for 6 h at 100 μg/vial resulted in significant antagonism of fipronil toxicity (LC50 = 4.39 ng a.i./cm2), whereas preexposure to PBO at 1 μg/vial had no effect (LC50 = 2.91 ng a.i./cm2). Fifth instars topically treated with 10 μg of PBO caused significant antagonism of fipronil toxicity (LD50 = 34.41 ng/insect). Electrophysiological recordings of spontaneous electrical activity were conducted on isolated ventral nerve cords from fifth instar larvae. Results from these experiments indicate that fipronil and its sulfone metabolite both reverse the inhibitory effect of GABA on spontaneous electrical activity. Fipronil, however, caused an increase in spontaneous electrical activity relative to that of the sulfone metabolite.