A way to turn off the ability to feel cold in mice was recently developed by neuroscientists at the University of Southern California.
The experts isolated chills at a cellular level, establishing the sensory network of neurons in the skin that relays the cold sensation.
Although the ability to sense cold in mice was shut off, the researchers, led by David McKemy, associate professor of neurobiology at the USC Dornsife College of Letters, Arts and Sciences, were able to allow the animals to still sense heat and touch.
A link between the experience of cold and a protein referred to as TRPM8, that in humans is encoded by the TRPM8 gene, was discovered in McKemy’s previous research. TRPM8 is a sensor of cold temperatures in neurons in the skin. It is also a receptor for menthol, the cooling component of mint.
Previous research indicated that the discovery of the cold sensation gene TRPM8 was important, because it is the single gene responsible for most cool temperature sensation.
In the new study, published in The Journal of Neuroscience, McKemy and his team isolated and ablated the neurons that express TRPM8 so that they could analyze the function of these cells particularly.
The researchers placed mice without TRPM8 neurons and control mice on a multi-temperature surface. Mouth-tracking software created by a student of McKemy was used to test their reactions.
The mice moved freely across the temperature surface, which ranged from 0 degrees to 50 degrees Celsius (32 to 122 degrees Farenheit).
According to the scientists, the mice that could not feel cold were the ones depleted of TRPM8 neurons. They could, however, still respond to heat.
The authors explained:
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.
There was no difference between the control mice and the mice without TRPM8-expressing neurons in tests of grip strength – responses to touch or coordinated movements.
The authors believe that their findings may pave the way for pain-relieving medications that do not undermine our ability to sense heat and touch.
McKemy concluded:
“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. 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.”
Written by Sarah Glynn