A hot pepper can make your tongue feel like it's on fire. That's because a receptor, at least in cultured cells, responds both to heat and a chili pepper ingredient. Now, scientists have demonstrated that mice lacking the receptor are less sensitive to high heat and other pain-inducing tests--a finding that may aid in the development of new pain-killing drugs.
Previous findings had strongly suggested that the so-called vanilloid receptor 1 (VR1) was important in feeling pain. The receptor allows nerve cells to respond to two classic pain stimuli: heat and capsaicin, the active ingredient in chili peppers. But cells don't experience pain. To prove that VR1 also played a role in living animals, researchers from the University of California, San Francisco (UCSF), and the University of Würzburg, Germany, produced a knockout mouse that lacked the corresponding gene.
The mice behaved normally in most respects, but when the researchers injected capsaicin into their hind paw--a treatment that causes normal mice to lick and shake the tender paw--they barely reacted, and their paws did not swell or become inflamed. They also drank happily from water spiced with capsaicin, which normal mice stayed clear of after a single sip. Furthermore, the mutant animals tolerated high heat better, including having their tails immersed in a hot water bath and their paws put in contact with a hot plate.
The results, published in the 14 April Science , show that the receptor is not only "an essential part of vanilloid sensitivity" but also plays an important role in several other kinds of pain, says UCSF team member David Julius. Indeed, neurosurgeon James Campbell of The Johns Hopkins University School of Medicine says that the receptor is a promising drug target. "If we go after these receptors, we may be able to control [certain kinds of] pain," he says.