The sting of the "potentially deadly" bark scorpion would be enough to make any human rile in pain, but the predatory grasshopper mouse brushes it off as if it were nothing.
If the mouse gets stung while hunting the creepy-crawler, it simply licks the area and continues to pursue its prey, a University of Michigan news release reported.
For these peculiar mice, the scorpion's venom acts as a painkiller instead of a pain stimulant. The southwestern U.S. mice are oddly resistant to the venom that could easily kill other animals.
"This venom kills other mammals of similar size," Ashlee Rowe, Michigan State University assistant professor of neuroscience and zoology, said. "The grasshopper mouse has developed the evolutionary equivalent of martial arts to use the scorpions' greatest strength against them."
The team injected small amounts of bark scorpion venom into the mice to see how the reacted. They also injected saline solution into the paws of a "control group" of mice. They noticed the mice licked their paws (which is the expected toxin response) for both the toxic and non-toxic injections.
"This seemed completely ridiculous," Harold Zakon, UT Austin professor of neuroscience, said. "One would think that the venom would at least cause a little more pain than the saline solution. This would mean that perhaps the toxin plays a role as an analgesic. This seemed very far out, but we wanted to test it anyway."
The team found the scorpion venom acts as a painkiller by "binding to sodium channels in the mouse pain neurons." This blocks the pain neuron from sending a signal to the rodent's brain.
"Pain neurons have a couple of different sodium channels, called 1.7 and 1.8, and research has shown that when toxins bind to 1.7 channels, the channels open, sodium flows in and the pain neuron fires," the news release reported.
The team sequenced genes for both sodium channels, and found that grasshopper mice had different amino acids in their 1.8 channel than in animals affected by the sting, including humans.
The scorpion toxin binds to one of these amino acids and blocks the 1.8 channel, stopping the pain response in its tracks.
"Incredibly, there is one amino acid substitution that can totally alter the behavior of the toxin and block the channel," Zakon said.
The team will need to perform further research in order to completely understand how the process works.
"We know the region of the channel where this is taking place and the amino acids involved," she said. "But there's something else that's playing a role, and that's what I'm focusing on next."
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