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.
January 25, 2013
Migraine sufferers know that a variety of influences—everything from stress to hunger to a shift in the weather—can trigger a dreaded headache. A new study published yesterday in the journal Cephalalgia, though, suggests that another migraine trigger could be an unexpected atmospheric condition—a bolt of lightning.
As part of the study, Geoffrey Martin of the University of Cincinnati and colleagues from elsewhere asked 90 chronic migraine sufferers in Ohio and Missouri to keep detailed daily diaries documenting when they experienced headaches for three to six months. Afterward, they looked back over this period and analyzed how well the occurrence of headaches correlated with lightning strikes within 25 miles of the participants’ houses, along with other weather factors such as temperature and barometric pressure.
Their analysis found that there was a 28 precent increased chance of a migraine and a 31 precent chance of a non-migraine (i.e. less severe) headache on days when lightning struck nearby. Since lightning usually occurs during thunderstorms, which bring a host of other weather events—notable changes in barometric pressure—they used mathematical models to parse the related factors and found that even in the absence of other thunderstorm-related elements, lightning alone caused a 19 percent increased chance of headaches.
Despite these results, it’s probably a bit premature to argue that lightning is a definitive trigger of migraines. For one, a number of previous studies have explored the links between weather and migraine headaches, and the results have been unclear. Some have suggested that high pressure increases the risk of headaches, while others have indicated that low pressure increases the risk as well. Other previous studies, in fact, have failed to find a link between migraines and lightening, in particular.
This study’s results are still intriguing, though, for a few reasons. One key element of the study was that, instead of using instances of lightning as reported by individuals on the ground, the researchers relied upon a series of ground sensors that automatically detect lightning strikes in the areas studied with a 90 percent accuracy. The researchers say this level of precision improves upon previous research and makes their results more indicative of the actual weather outside.
The study also looked at the polarity of lightning strikes—the particular electrical charge, whether positive or negative, that a bolt of lightning carries as it surges from the clouds to the ground—and found that negatively charged lightning strikes had a particularly strong association with migraines.
The researchers don’t have a clear explanation yet for how lightning might play a role, but they mention a wide variety of possibilities. ”There are a number of ways in which lightning might trigger headaches,” Martin said. “Electromagnetic waves emitted from lightning could trigger headaches. In addition, lightning produces increases in air pollutants like ozone and can cause release of fungal spores that might lead to migraine.”
January 16, 2013
Can crabs feel pain? New research on the clawed crustaceans suggests the answer is yes.
A group of UK researchers came to this conclusion by examining the reactions of common shore crabs to mild electric shocks in a study released today in the Journal of Experimental Biology. The key to their finding is the distinction between the nervous system activity known as nociception and pain, which is defined as an unpleasant sensory and emotional experience. For years, many researchers assumed crustaceans such as crabs experienced the former, but not the latter.
Nociception—which differs from pain in that it isn’t subjective—is produced by the peripheral and central nervous systems in reaction to potentially tissue-damaging stimuli. All animals experience this reflex, including humans—for example, the nerve endings (called nociceptors) under our skin transmit a signal along our spinal cord to the brain when we touch a too-hot plate, and we automatically jerk our hands back.
For crabs, nociception provides immediate protection following a small electric shock, but it shouldn’t trigger any changes in its later behavior. That’s a job for pain—it helps organisms learn to avoid the harmful source in the future.
In this study, the crabs appeared to do just that. Ninety crabs were placed in a tank with two areas without a light source, one crab at a time. After the crabs scuttled toward the dark area they liked best, they were removed from the tank and exposed to a mild electric shock.
Following a rest period, each of the crabs was returned to the tank. Most of the crustaceans returned to the shelter they’d picked the first time. Those who had received a shock in the first round were zapped again, and when they were introduced into the tank for the third time, the majority moved to the other, presumably shock-free safe area. Crabs who hadn’t been shocked returned once again to their first-choice area.
Dark hideaways, like under rocks along waterbeds, are important to these creatures because they offer protection from predators. After receiving the electric shocks, the decapods chose to trade in safety to avoid the unpleasant experience in the future.
“Having experienced two rounds of shocks, the crabs learned to avoid the shelter where they received the shock,” said study co-author Bob Elwood, an animal behavior professor at the School of Biological Sciences at Queen’s University Belfast, in a statement. “They were willing to give up their hideaway in order to avoid the source of their probable pain.”
So did the crabs remember the pain? The researchers say it’s possible, and previous work by Elwood and others supports the idea.
In a 2009 study with hermit crabs, wires attached to the creatures’ shells delivered small shocks to their abdomens, which they typically protect by crawling into empty mollusk shells. The only crabs to abandon their shells in search of others had previously incurred electric shocks, which researchers say means the crabs found the experience unpleasant—and perhaps ouch-worthy.
A new shell was then offered, and those crabs that had been shocked but remained in their original homes moved quickly toward the new option, investigated it for a shorter time and were more likely to make the switch than those who hadn’t been shocked. Experiencing shocks changed the hermit crabs’ motivation, much like the way we choose not to touch that hot plate again.
Such behavioral changes were also the subject by a 2007 paper by Elwood, with a different crustacean, the prawn. Various noxious stimuli introduced to prawns’ antennae elicited a reflexive tail flick. But after that, the prawns groomed their antennae and rubbed them against the side of their tanks, prolonged activities that, researchers say, signal the experience of pain.
While it’s impossible to explicitly demonstrate that crustaceans like crabs, prawns and lobsters feel pain, researchers hope these findings spur investigation of how the marine animals are handled in aquaculture and in the kitchen, where chefs often declaw or boil crabs alive.
December 20, 2012
One of the chief arguments for the legalization of medicinal marijuana is its usefulness as a pain reliever. For many cancer and AIDS patients across the 19 states where medicinal use of the drug has been legalized, it has proven to be a valuable tool in managing chronic pain—in some cases working for patients for which conventional painkillers are ineffective.
To determine exactly how cannabis relieves pain, a group of Oxford researchers used healthy volunteers, an MRI machine and doses of THC, the active ingredient in marijuana. Their findings, published today in the journal Pain, suggest something counterintuitive: that the drug doesn’t so much reduce pain as make the same level of pain more bearable.
“Cannabis does not seem to act like a conventional pain medicine,” Michael Lee, an Oxford neuroscientist and lead author of the paper, said in a statement. “Brain imaging shows little reduction in the brain regions that code for the sensation of pain, which is what we tend to see with drugs like opiates. Instead, cannabis appears to mainly affect the emotional reaction to pain in a highly variable way.”
As part of the study, Lee and colleagues recruited 12 healthy volunteers who said they’d never used marijuana before and gave each one either a THC tablet or a placebo. Then, to trigger a consistent level of pain, they rubbed a cream on the volunteers’ legs that included 1% capsaicin, the compound found that makes chili peppers spicy; in this case, it caused a burning sensation on the skin.
When the researchers asked each person to report both the intensity and the unpleasantness of the pain—in other words, how much it physically burned and how much this level of burning bothered them—they came to the surprising finding. “We found that with THC, on average people didn’t report any change in the burn, but the pain bothered them less,” Lee said.
This indicates that marijuana doesn’t function as a pain killer as much as a pain distracter: Objectively, levels of pain remain the same for someone under the influence of THC, but it simply bothers the person less. It’s difficult to draw especially broad conclusions from a study with a sample size of just 12 participants, but the results were still surprising.
Each of the participants was also put in an MRI machine—so the researchers could try to pinpoint which areas of the brain seemed to be involved in THC’s pain relieving processes—and the results backed up the theory. Changes in brain activity due to THC involved areas such as the anterior mid-cingulate cortex, believed to be involved in the emotional aspects of pain, rather than other areas implicated in the direct physical perception of it.
Additionally, the researchers found that THC’s effectiveness in reducing the unpleasantness of pain varied greatly between individuals—another characteristic that sets it apart from typical painkillers. For some participants, it made the capsaicin cream much less bothersome, while for others, it had little effect.
The MRI scans supported this observation, too: Those more affected by the THC demonstrated more brain activity connecting their right amydala and a part of the cortex known as the primary sensorimotor area. The researchers say that this finding could perhaps be used as a diagnostic tool, indicating for which patients THC could be most effective as a pain treatment medicine.