USC research on cold sensitivity could help control pain in future
Researchers at USC have made mice insensitive to near-freezing temperatures by deactivating select neurons, a development that could one day lead to new treatments for pain in humans.
In a study published Tuesday in the Journal of Neuroscience, researchers used a bacterial toxin to kill neurons equipped with so-called TRPM8 channels, cellular structures that help relay sensations of cold. (The pathway is also responsible for sensing menthol, the cooling component of mint.) Neurons that sense heat and mechanical pain were left intact, however.
The mice with the dead, or ablated, neurons were exposed to a variety of stimuli and compared with normal mice.
In one test, the mice were placed on a multi-temperature surface. As different areas of the surface fluctuated between freezing and 122 degrees Fahrenheit, the movement of each mouse was tracked.
The altered mice were far more likely than normal mice to stay put on surfaces that grew progressively, and dangerously colder. The altered mice, however, were inclined to move away from those surfaces that grew increasingly hot, just like normal mice.
Lead study author David McKemy, associate professor of neurobiology at USC Dornsife College of Letters, Arts and Sciences, said that by narrowing in on sensations at the molecular level, doctors might one day treat pain with more precision.
“The problem with pain drugs now is that they typically just reduce inflammation, which is just one potential cause of pain, or they knock out all sensation, which often is not desirable,” McKemy said in a news release. “One of our goals is to pave the way for medications that address the pain directly, in a way that does not leave patients completely numb.”
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