A type of mouse native to the US southwest eats toxic scorpions to feel better.
The venom from the bark scorpion can kill other animals, but it acts as a painkiller for grasshopper mice. When stung, grasshopper mice briefly lick their paws and move in again for the kill.
“This venom kills other mammals of similar size,” says Ashlee Rowe, lead author of the paper published in Science and assistant professor of neuroscience and zoology at Michigan State University. “The grasshopper mouse has developed the evolutionary equivalent of martial arts to use the scorpions’ greatest strength against them.”
‘This seemed very far out’
Rowe, who conducted the research while at the University of Texas at Austin, and her colleagues ventured into the desert and collected scorpions and mice for their experiments.
To test whether the grasshopper mice felt pain from the toxin, the scientists injected small amounts of scorpion venom or nontoxic saline solution in the mice’s paws. Surprisingly, the mice licked their paws (a typical toxin response) much less when injected with the scorpion toxin than when injected with a nontoxic saline solution.
“This seemed completely ridiculous,” says Harold Zakon, UT Austin professor of neuroscience. “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.”
Blocks pain signal
Rowe and Zakon discovered that the bark scorpion toxin acts as an analgesic by binding to sodium channels in the mouse pain neurons, and this blocks the neuron from firing a pain signal to the 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.
By sequencing the genes for both the 1.7 and 1.8 sodium channels, the scientists discovered that channel 1.8 in the grasshopper mice has amino acids different from mammals that are sensitive to bark scorpion stings, such as house mice, rats, and humans.
They then found that the scorpion toxin binds to one of these amino acids to block the activation of channel 1.8 and thus inhibit the pain response.
“Incredibly, there is one amino acid substitution that can totally alter the behavior of the toxin and block the channel,” Zakon says.
Help for humans?
The riddle hasn’t been completely solved just yet, though, Rowe says.
“We know the region of the channel where this is taking place and the amino acids involved,” she adds. “But there’s something else that’s playing a role, and that’s what I’m focusing on next.”
Some resistance to prey toxins in mammals has been found in other species. The mongoose, for example, is resistant to the cobra. And naked mole rats’ eyes do not burn in pain when carbon dioxide builds up in their underground tunnels.
This study, however, is the first to find that an amino acid substitution in sodium channel 1.8 can have an analgesic effect.
Rowe says studies such as this could someday help researchers target these sodium channels for the development of analgesic medications for humans.
Additional researchers from Indiana University School of Medicine and Michigan State contributed to the study.