Researchers at University of Southern California report that they have identified a specific protein receptor that is responsible for the mediation of cold-related pain. The discovery may lead to the development of new therapies for cold allodynia—pain caused by cold sensitivity—for which there a few available options at present. Allodynia can be induced by neuropathy from chemotherapy, diabetes, and other conditions, as well as from injury. The protein, called glial cell-line derived neurotrophic factor receptor α3 (GFRα3), controls the ability of nerve cells to transmit cold-related pain signals after an injury. The study was published online earlier this month by Proceedings of the National Academy of Sciences.
The immune response to injury involves the release of various substances that cause inflammation. Some of the compounds in this “inflammatory soup” make sensory neurons more sensitive to stimuli after the injury. While sensitivity to pressure or heat have been previously studied, this research with genetically-engineered mice is the first to pinpoint GFRα3 as responsible for mediating cold sensitization after an injury. According to lead author David McKemy, PhD, the findings point to therapeutic drug targets that may be possible to develop. "One of the things that people don't appreciate is how allodynia related to these traumatic neuropathies—these issues such as chemotherapy or nerve injury or diabetes issues—are actually reported almost as prevalently as sensitivity to heat and mechanical."
Read more about the research findings here.
The journal abstract may be read here.