Professors Develop Cold Sensor Shutoff
Associate Professor of Neurobiology David McKemy and his team have developed a toxin that was injected into full grown mice. The toxin shuts off receptors that sense a surface or tempurature that is dangerously cold.
The toxin targets the neurons in the skin that sense cold which are called TRPM8 (pronounced trip-em-ate), then destroyed the cold-sensing function. TRPM8 is also the component in mint to make it seem cool.
By isolating these neurons in mice, McKemy and his team have been able to examine the functions of these receptors and better understand how they can be turned off.
Two sets of mice, one with the toxin and one without, were put onto a surface that had three levels of heat from 32 degrees Farenheit to 122 degrees Farenheit.
The group of mice that were depleted of the TRPM8 avoided the hot suface but were not afraid of the surfaces that were between 32 to 85 degrees Farenheit. The mice that were not given the toxin and able to sense the cold stayed on the 85 degrees surface during the whole test period.
The overall idea helps to better understand how the system changes after an injury and how the body responds to cold, with an aim to developing treatments.
"Most drugs that are used for pain relief do not target specifically at perception," said McKemy.
