USC neuroscientists have isolated the sensory network of neurons in the skin that relays the sensation of cold. David McKemy, associate professor of neurobiology at the USC Dornsife College of Letters, Arts and Sciences, and his team have succeeded at selectively shutting off the ability to sense cold in mice while still leaving them able to sense heat and touch. McKemy and his co-authors, all of USC, published their findings in The Journal of Neuroscience on Feb. 13.
McKemy had previously discovered a link between the sensation of cold and a protein known as TRPM8, which is a sensor of cold temperatures in neurons in the skin, as well as a receptor for menthol, the cooling component of mint.
Using mouse-tracking software program developed by one of McKemy’s students, the researchers tested control mice and mice without TRPM8 neurons on a multi-temperature surface. The surface temperature ranged from 0 degrees to 50 degrees Celsius (32 to 122 degrees Farenheit), and mice were allowed to move freely among the regions.
Control mice tended to stick to an area around 30 degrees Celsius (86 degrees Fahrenheit) and avoided both colder and hotter areas. But mice without TRPM8 neurons avoided only hotter plates and not cold, even when the cold should have been painful or was potentially dangerous.
By better understanding the specific ways in which people feel sensations, scientists may one day develop better pain treatments that don't blot out all ability to feel any sensations.
“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. “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.”