A venomous bark scorpion, its stinger poised to strike, confronts a furry, little grasshopper mouse somewhere in the desert. A deadly melee is about to begin and you won’t believe who wins.

Even though the bark scorpion possesses one of the most painful -- and potentially lethal -- stings in the animal kingdom, he’s about to become lunch for a twitchy little rodent.

Thanks to evolution, the grasshopper mouse no longer feels the intense burning, and subsequent throbbing, that humans or other mice feel when injected with scorpion venom -- pain that would stop most predators dead in their tracks.

In fact, after several stings to the face, a grasshopper mouse stops briefly to groom itself, then resumes its savage attack before feasting on the overwhelmed scorpion.


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

In a paper published recently in the journal Science, Rowe and colleagues investigated how it was that grasshopper mice were able to switch off this intense pain. After all, pain is essential for survival. Without it, organisms suffer repeated injury and perhaps premature death.

What they found was a modification to mouse pain receptors that made the toxin function as a pain reliever instead of a pain stimulant. However, scientists said they remained stumped as to why the venom failed to kill the mice.

To investigate the phenomenon, researchers traveled to the Arizona desert to collect bark scorpion and grasshopper mouse specimens. Back in the lab, they wanted to see if the mice felt no pain at all, or only blocked pain from the venom.


They used a needle and syringe to inject either scorpion venom or saline solution into the feet of the mice. They were surprised to find that the mice showed a greater pain response -- licking of the injection site -- after being shot up with the saline.

“This seemed completely ridiculous,” Harold Zakon, a professor of neuroscience at the University of Texas at Austin, said in a prepared statement.

“One would think that the venom would at least cause a little more pain than the saline solution,” Zakon said. “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.”

Researchers turned their attention to mouse nociceptors, nerve cells that respond to specific stimuli and then fire messages to the spinal cord and brain. They can respond to temperature, chemicals, or physical damage.


Mammal nociceptors are equipped with a variety of so-called voltage-gated sodium channels, which respond to specific stimuli. When a channel opens, sodium flows in and causes the pain neuron to fire a message to the brain: OUCH!

In humans and most mice, bark scorpion venom induces pain by activating the sodium ion channel, or NAV 1.7, but not NAV 1.8.

Researchers found that in grasshopper mice, NAV 1.8 has an unusual amino acid that binds to the toxin and blocks sodium currents.

Study authors say they still have questions about what exactly is happening in the mice, but that the answer could have far reaching implications for the treatment of pain in humans.


“The molecular and biochemical interactions between venom peptides and NAV 1.8 could serve as the basis for designing highly selective, nonaddictive analgesics,” authors concluded.

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