Grasshopper Mouse Impervious to Bark Scorpion Sting

The pain of a bark scorpion sting is lost on grasshopper mice, which prey on the small arachnids. Rather, the toxin released by the sting acts as an analgesic instead of a pain stimulant, a study published in the journal Science found.

"This venom kills other mammals of similar size," Ashlee Rowe, a Michigan State University assistant professor of neuroscience and zoology, said in a statement. "The grasshopper mouse has developed the evolutionary equivalent of martial arts to use the scorpions' greatest strength against them."

Rowe, who conducted the study while at the University of Texas, ventured into the desert to collect the scorpions and mice. Then, in order to determine whether the mice felt pain when treated with the toxin, they injected small amounts of it into the mice's paws along with a nontoxic saline solution. Rowe and her colleagues were stunned when the mice responded to the saline solution far more than the other.

"This seemed completely ridiculous," said Harold Zakon, a 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."

The scientists discovered that the bark scorpion binds to sodium channels in the mouse pain neurons, blocking the neuron from firing a pain signal to the brain.

Pain neurons are able to use a couple of different sodium channels, called 1.7 and 1.8. Research shows that when toxins bind with 1.7 channels, they open, sodium enters and the pain neuron fires. By sequencing the genes for 1.7 and 1.8 channels, the researchers found that, in the case of the grasshopper mouse, the latter has different amino acids than those mammals that are sensitive to scorpion stings.

Next they discovered that the toxin binds to one of these amino acids in order to keep the 1.8 channel from activating.

"Incredibly, there is one amino acid substitution that can totally alter the behavior of the toxin and block the channel," Zakon said.

Going forward, Rowe said, "We know the region of the channel where this is taking place and the amino acids involved. But there's something else that's playing a role, and that's what I'm focusing on next."