Animals use their sensory systems to navigate their environment and to mediate interactions with other animals. Traits that mediate interactions between predator and prey rely on fast, specialized sensory inputs. Ion channels expressed in excitable membranes are critical for encoding information about and producing responses to sensory stimuli. Given the critical role of ion channels in transmitting neuronal signals and producing muscle contractions, it is not surprising that some animals have evolved toxins that bind ion channels and disrupt their activity. Toxin producers use their chemical weapons to subdue prey and to deter predators. Toxins that induce intense pain provide prey with the opportunity to escape – and if the encounter is particularly unpleasant – the predator may learn to avoid that prey species. However, pain-inducing toxins that produce both immediate and long-term behavioral modification may impose strong selection on the receiver, potentially driving the evolution of counter adaptations that mediate interactions between toxin producers and their enemies. My goal is to understand how receivers respond to these selection pressures. Specifically, I want to determine the effects of toxins on the structure and function of ion channels expressed in somatosensory neurons that mediate the sensation of pain, and, ultimately, understand how changes in ion channels feed back on and influence predatory, foraging and feeding behavior. Bark scorpions (Centruroides spp.) produce toxins that selectively bind sodium- (Na+) ion channels expressed in peripheral pain-pathway neurons (nociceptors), inducing intense pain in sensitive mammals. Grasshopper mice (Onychomys spp.), predators of bark scorpions, have evolved resistance to their venom. Behavioral assays demonstrated that grasshopper mice are insensitive to bark scorpion pain-inducing toxins. Recordings of Na+ current from channels expressed in grasshopper mice’s nociceptors revealed a novel mechanism where a component of bark scorpion venom is co-opted by these Na+ channels – to block the very pain signals that the toxins are generating. Cloning and sequencing of genes that encode nociceptor-expressed Na+ channels from grasshopper mice revealed structural modifications in the channel that are positioned to co-opt toxin activity. Current work is focused on using site-directed mutagenesis, an expression system and electrophysiology to determine if structural modifications of grasshopper mice Na+ channels produce functional changes in nociceptors that explain insensitivity to bark scorpion pain-inducing toxins.