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SUMMARY:No pain, big gain: coevolution between bark scorpion pain-inducing 
 toxins and grasshopper mouse nociceptors
LOCATION:Anatomy/Zoology Building W118
TZID:America/Denver
DTSTART:20120001T000000
UID:2026-04-23-09-52-52@natsci.colostate.edu
DTSTAMP:20260423T095252
Description:Animals use their sensory systems to navigate their environment
  and to mediate interactions with other animals.  Traits that mediate int
 eractions between predator and prey rely on fast\, specialized sensory inp
 uts.  Ion channels expressed in excitable membranes are critical for enco
 ding information about and producing responses to sensory stimuli.  Given
  the critical role of ion channels in transmitting neuronal signals and pr
 oducing 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 e
 scape – and if the encounter is particularly unpleasant – the predator
  may learn to avoid that prey species.  However\, pain-inducing toxins th
 at produce both immediate and long-term behavioral modification may impose
  strong selection on the receiver\, potentially driving the evolution of c
 ounter adaptations that mediate interactions between toxin producers and t
 heir enemies.  My goal is to understand how receivers respond to these se
 lection pressures.  Specifically\, I want to determine the effects of tox
 ins on the structure and function of ion channels expressed in somatosenso
 ry neurons that mediate the sensation of pain\, and\, ultimately\, underst
 and how changes in ion channels feed back on and influence predatory\, for
 aging and feeding behavior.  Bark scorpions (Centruroides spp.) produce t
 oxins that selectively bind sodium- (Na+) ion channels expressed in periph
 eral pain-pathway neurons (nociceptors)\, inducing intense pain in sensiti
 ve mammals.  Grasshopper mice (Onychomys spp.)\, predators of bark scorpi
 ons\, have evolved resistance to their venom.  Behavioral assays demonstr
 ated 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 pa
 in signals that the toxins are generating.  Cloning and sequencing of gen
 es that encode nociceptor-expressed Na+ channels from grasshopper mice rev
 ealed structural modifications in the channel that are positioned to co-op
 t toxin activity.  Current work is focused on using site-directed mutagen
 esis\, an expression system and electrophysiology to determine if structur
 al modifications of grasshopper mice Na+ channels produce functional chang
 es in nociceptors that explain insensitivity to bark scorpion pain-inducin
 g toxins. 4:00 pm
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