January 14, 2020 8:20 am

From the day they are born, grasshopper mice are natural killers. Even pups born and raised in captivity quickly figure out how to take down prey much larger than themselves. They appear to learn some of their aggression from their fathers: pups raised with two parents are more likely to bully other mice and attack insects more viciously than those raised by single mothers.

Their manners don’t improve with age. Rather than making their own nests, grasshopper mice take over burrows built by other rodents, removing the occupants by force if necessary.

In tough times, the mice will kill and eat other rodents, even those of their own species. Naturalists tell of finding a circus of different flea species on the animals; seemingly souvenirs from their various victims.

Venom? Pah!

But perhaps more interesting than their cannibalism is their resistance to the venom of the Arizona bark scorpions (Centruroides sp) that share their desert. Among the most poisonous scorpions in the world, Centruroides’ painful venom causes muscle contractions and respiratory failure in humans. Yet grasshopper mice kill and eat them without pause.

To discover their secret, Ashlee Rowe of Sam Houston State University in Huntsville, Texas, and colleagues injected a very small amount of scorpion venom into the paw of a grasshopper mouse and a standard-issue lab mouse (Mus musculus). The grasshopper mouse spent far less time licking its paw, suggesting that the venom was less painful to it.

The team then removed individual nerve cells from the mouse’s spinal cord that convey pain signals to the brain, and measured how the venom altered their function. Normally, scorpion venom activates a protein in the cell membrane called Nav1.7 that makes it fire pain signals. But grasshopper mice, they found, have a mutation in a different protein, Nav1.8, that prevents the signal from travelling any further and reaching the brain. Rowe presented the group’s findings at the Society for Integrative and Comparative Biology meeting in San Francisco last week.

In humans, Rowe says, mutations in Nav1.7 cause a syndrome called erythromelalgia. In this disease, a characteristic burning pain in the feet and hands crops up spontaneously. The researchers are now attempting to figure out exactly how the mouse’s mutation in Nav1.8 blocks pain signals, to see if it could help design a new kind of pain killer.

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This post was written by Nadia Vella