Now they have demonstrated that the receptor does indeed detect heat by examining the physiological and behavioral characteristics of a knockout mouse with no TRPV3 proteins. The mice appear completely normal behaviorally except that they have severe deficiencies in their ability to detect warm and hot temperatures. Patapoutian and his colleagues also showed that, in cultured keratinocyte cells, TRPV3 is activated by the compound camphor, which is one of the main ingredients in many warming rubs. TRPV3 is the first known receptor for camphor.
Significantly, when Patapoutian and his colleagues discovered TRPV3 a few years ago, they were intrigued to discover that it is unique among thermoTRP channels in that it is expressed on the surface of skin cells known as keratinocytes. At the time, they hypothesized that its presence on keratinocytes might mean that the detection of temperature takes place in the skin as well as on these neurons.
In their Science paper, they demonstrate that this is indeed the case by showing that camphor activates TRPV3 on keratinocytes but not on sensory neurons. In the knockout models, this heat- and camphor-mediated activity disappears, which suggests that it is the TRPV3 proteins on the keratinocytes that are actually detecting warm temperatures. It is not known how this signal is communicated to the brain, since keratinocytes, unlike neurons, have no direct link with the central nervous system. Keratinocytes do, however, touch nerve fibers, and it may be through these contacts that the signals are communicated. Investigations into this possibility are ongoing.
To read the article, "Impaired Thermosensation in Mice Lacking TRPV3, a Heat and Camphor Sensor in the Skin" by Aziz Moqrich, Sun Wook Hwang, Taryn J. Earley, Matt J. Petrus, Amber N. Murray
Source:Scripps Research Institute