Carnivorous grasshopper mice (Onychomys) and their chemically-defended prey (scorpions, darkling beetles, centipedes, tarantulas) provide a powerful, ecologically relevant model for examining the role of ion channels in sensory and neuromuscular adaptations that mediate predatory behavior.

Neurotoxins that target sensory neurons and muscle cells offer a unique opportunity to explore the molecular mechanisms by which animals transduce sensory stimuli into electrical signals, interpret signals, and generate motor responses. We use scorpion venom toxins and noxious beetle sprays for studying the proteins (ion channels) expressed in sensory neurons that encode information about external stimuli and in muscle cells that regulate responses to that information.

Bark scorpions (Centruroides) produce toxins (peptides) that bind ion channels, disrupting nerve signaling and muscle contraction. Toxins that bind sensory neurons cause burning pain, and sensitivity to touch, pressure and temperature. The toxins do not cause tissue damage; they bind sodium (Na+) and potassium (K+) ion channels in sensory neurons that regulate responses to chemical, mechanical and thermal stimuli. Thus, the toxins are excellent tools for probing the structure and function of ion channels in sensory neurons, and for exploring how channels work together to regulate neuronal excitability.

Darkling beetles (Eleodes) produce an acidic cocktail containing benzoquinones that they spray in the face of their predators causing irritation of the eyes, mouth, upper and lower airways. The spray activates TRPA1 and TRPV1 expressed in sensory neurons, which then initiates an inflammatory response in sensitive animals.

Grasshopper mice, predators of bark scorpions and darkling beetles, have evolved resistance to painful venom peptides and beetle sprays via modifications to their sensory ion channels. The mice provide an ideal model to study sensorimotor processes and behavior because they exhibit differential sensory and neuromuscular phenotypes that can be linked to genetic variation in ion channel genes.