No pain, big gain: coevolution between bark scorpion pain-inducing toxins and grasshopper mouse nociceptors

Field: Neuroscience (Life Sciences)

Event Abstract Back to Event No pain, big gain: coevolution between bark scorpion pain-inducing toxins and grasshopper mouse nociceptors Ashlee H. Rowe1*, Yucheng Xiao2, Matthew Rowe3, Theodore Cummins2 and Harold Zakon1 1 The University of Texas at Austin, Section of Neurobiology, United States 2 Indiana University Medical School, Pharmacology/Toxicology, United States 3 Sam Houston State University, Department of Biology, United States 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). Bark scorpion venom induces 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 the nociceptor 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. Keywords: evolution of resistance to pain, grasshopper mice, Na+ ion channels, Neurotoxins, predator-prey interactions, scorpion venom, somatosensory pain Conference: Tenth International Congress of Neuroethology, College Park. Maryland USA, United States, 5 Aug - 10 Aug, 2012. Presentation Type: Poster (but consider for Participant Symposium) Topic: Sensory: Mechanosensation Citation: Rowe AH, Xiao Y, Rowe M, Cummins T and Zakon H (2012). No pain, big gain: coevolution between bark scorpion pain-inducing toxins and grasshopper mouse nociceptors. Conference Abstract: Tenth International Congress of Neuroethology. doi: 10.3389/conf.fnbeh.2012.27.00052 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 02 May 2012; Published Online: 07 Jul 2012. * Correspondence: Dr. Ashlee H Rowe, The University of Texas at Austin, Section of Neurobiology, Austin, TX, 78705, United States, ahrowe@mail.utexas.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ashlee H Rowe Yucheng Xiao Matthew Rowe Theodore Cummins Harold Zakon Google Ashlee H Rowe Yucheng Xiao Matthew Rowe Theodore Cummins Harold Zakon Google Scholar Ashlee H Rowe Yucheng Xiao Matthew Rowe Theodore Cummins Harold Zakon PubMed Ashlee H Rowe Yucheng Xiao Matthew Rowe Theodore Cummins Harold Zakon Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.