The vanilloid-1 receptor, now known as the transient receptor potential vanilloid-1 receptor is activated by capsaicin, the drug injected subcutaneously by scientists in an attempt to study C fiber sensitization. Vanilloids include its potential to bind to cannabinoids. However, TRPV-1 binds to many other substances such as capsaicin, resiniferatoxin, etc.
TRPV-1 now appears to sit at a crossroads. The little receptor, which is tied in with calcium metabolism pathways turns out to have an active role in two very important areas. It appears to play a central role in initiating inflammatory responses AND integrating painful stimuli. See Veronesi B and Ooortgiesen M Toxicol Sci. 2006 Jan;89(1):1-3. It has recently been discovered that when TRPV-1 is blocked, cellular receptor proteins for it increase markedly. This is bizarre. The cell is actually on the lookout for TRPV. Why would a cell be searching for inflammation and pain. It also confuses us further on whether inflammation is part of pain, or whether pain is part of inflammation or neither. The body demonstrates over and over its economy by using identical chemicals to accomplish different tasks simply by producing receptors with different properties.
However, study of TRPV-1 has now moved into the environmental area, such as the two EPA scientists mentioned above at Research Triangle Park in North Carolina, who are concerned about toxic particles in the environment which suppress TRPV-1. It is tempting for the CP patient to ask if they could please have a double helping of whatever environmental toxins are suppressing TRPV-1. We could do with a little TRPV-1 antagonism. The environmentalists of course are concerned about suppression of the immune inflammatory response, making the public more susceptible to certain diseases and conditions. What is odd is that CP patients who are literally drowning in TRPV-1 activity have not yet been detected to possess any beneficial immunity, although they certainly have bucketloads of inflammation and pain.
It grows increasingly odd that TRPV-1 which is manifestly behind inflammation and pain, and which is inarguably much more active in central pain, is nevertheless insufficient evidence for some that central pain even exists. TRPV-1 either increases pain or it doesn’t. If it does, and CP subjects have lots of it, then why is there any remaining skepticism about the pain. Someone is just not reading the literature. Although the EPA is hardly worried about pain, if they can document cell surface proteins searching desperately for TRPV-1 to maintain proper immunity then why is Central Pain of no interest in studies of immunity. For one reason or another, CP is just simply not yet sufficiently intriguing to draw the proper funding. We hope this changes quickly. CP patients may have both increased TRPV-1 presence AND increased TRPV-1 sensitivity.