October 24, 2013
If you were stung by a bark scorpion, the most venomous scorpion in North America, you’d feel something like the intense, painful jolt of being electrocuted. Moments after the creature flips its tail and injects venom into your skin, the intense pain would be joined by a numbness or tingling in the body part that was stung, and you might experience a shortness of breath. The effect of this venom on some people—small children, the elderly or adults with compromised immune systems—can even trigger frothing at the mouth, seizure-like symptoms, paralysis and potentially death.
Based solely on its body size, the four-inch-long furry grasshopper mouse should die within minutes of being stung—thanks to the scorpion’s venom, which causes temporary paralysis, the muscles that allow the mouse to breathe should shut down, leading to asphyxiation—so you’d think the rodent would avoid the scorpions at all costs. But if you put a mouse and a scorpion in the same place, the rodent’s reaction is strikingly brazen.
If stung, the four-inch-long rodent might jump back for a moment in surprise. Then, after a brief pause, it’ll go in for the kill and devour the scorpion piece by piece:
This predatory behavior isn’t the result of remarkable toughness. As scientists recently discovered, the mouse has evolved a particularly useful adaptation: It’s immune to both the pain and paralytic effects that make the scorpion’s venom so toxic.
Although scientists long knew that the mouse, native to the deserts of the American Southwest, preys upon a range of non-toxic scorpions, “no one had ever really asked whether they attack and kill really toxic scorpions,” says Ashlee Rowe of Michigan State University, who led the new study published today in Science.
To investigate, Rowe visited the desert nearby Arizona’s Santa Rita Mountains and collected a number of mice and scorpions. Back at her lab, when she and colleagues put the two animals together in the same tank, they saw that the mice devoured the scorpions with gusto and were seemingly impervious to their toxic strings, showing no signs of inflammation or paralysis afterward. They even directly injected the venom into other mouse specimens to further confirm that it didn’t affect them physiologically.
The question remained, though, whether the mice were merely immune to the venom’s paralyzing effects, or were also unable to feel pain as a result of a sting. “I’d see the mice get stung, and they’d just groom a little bit and blow it off,” Rowe says. After she talked to people who’d been stung and heard how badly it hurt, she hypothesized that the mild reaction in the mice indicated that they were resistant to the pain itself.
Working with Yucheng Xiao and Theodore Cummins of Indiana University, she closely examined the physical structures that connect the sensory neurons (which convey external stimuli, such as pain) to the central nervous system (where pain is experienced). “There are big, long neurons that extend from the hands and feet all the way to the spinal cord, and they’re responsible for taking information from the environment and sending it to the brain,” she says.
Incredibly, the nerve cells associated with the interface between these two systems can continue functioning normally when they’ve been removed from the mice, if they’ve been properly preserved and cultured in a medium. As a result, her team was able to look at the mechanisms that control the flow of signals between the sensory neurons and the spinal cord—structures known as ion channels—and see if those present in grasshopper mice functioned differently than those in house mice when exposed to scorpion venom.
They found, in house mice, the venom caused a channel known as Nav1.7 to pass along a signal, causing the perception of pain. In grasshopper mice, though, something unexpected happened: The arrival of venom caused no change in the activity of Nav1.7, because proteins produced by a different ion channel, known as Nav1.8, bound to venom molecules and rendered them futile. In fact, this reaction produced an overall numbing effect on the entire mouse pain transmission system, leaving the animals temporary incapable of feeling all sorts of pain, including those unrelated to scorpion venom.
The researchers also looked at the underlying genetics, sequencing the genes that correspond to these alternatively-structured ion channels, which will allow them to investigate the specific evolutionary background of this remarkable adaptation. In theory, the incentives for the mouse species evolving an immunity to scorpion toxins seem obvious: The nocturnal rodent feeds on all sorts of scorpions, so unless it can visually distinguish between those that are benign and toxic, it will face severe consequences if it’s sensitive to the venom. “Death, after all, is a pretty strong selection pressure,” Rowe notes.
But on the other hand, pain serves a crucial evolutionary role, informing an organism when it’s in danger. Some other species have been know to evolve resistance to particular toxins (garter snakes, for instance, are resistant to the toxin produced by rough-skinned newts), but these examples all involve resistance to toxins that can kill, but don’t actually cause pain.
So the fact that grasshopper mice have evolved resistance to pain itself is novel—and likely a result of a very specific set of evolutionary circumstances. One important aspect is that bark scorpions are a significant proportion of the mouse diet, leading to frequent interactions between the two organisms. Additionally, says Rowe, “the mechanism is specific to the venom itself, so it doesn’t compromise the mouse’s overall pain pathways.” As a result, the mouse is still able to detect other sources of pain (just not right after it’s been bitten by by the scorpion), and thus will know when its faced with unrelated painful perils.
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