Meeting Abstract

105.6  Sunday, Jan. 6  No pain, big gain: coevolution between bark scorpion pain-inducing toxins and grasshopper mouse nociceptors ROWE, A.*; XIAO, Y.; ROWE, M.; CUMMINS, T.; ZAKON, H.; The Univ. of Texas at Austin; Indiana Univ. School of Medicine; Sam Houston State Univ.; Indiana Univ. School of Medicine; The Univ. of Texas at Austin

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 their critical role, it is not surprising that some animals have evolved toxins that bind ion channels and disrupt their activity. Disruption of channel activity may impose strong selection on the receiver, driving the evolution of counter adaptations. Arizona Bark scorpions [(AZB) (Centruroides sculpturatus)] produce toxins that selectively bind sodium- (Na+) ion channels expressed in pain-pathway neurons (nociceptors), inducing intense pain in sensitive mammals. Southern grasshopper mice [(SG) (Onychomys torridus)] attack and consume these toxic scorpions. Natural stings and paw-licking assays showed that SG mice respond only briefly to venom, suggesting they have evolved insensitivity to pain-inducing toxins. Recordings of Na+ current from ion channels expressed in SG mice nociceptors revealed a novel mechanism where a component of AZB 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.