Capsaicin, the active agent in spicy hot chili peppers, often acts as an irritant, but it may also be used to reduce pain.
Feng Qin, associate professor of physiology and biophysics at the University at Buffalo School of Medicine, and Jing Yao used capsaicin to unravel how pain-receptor systems can adapt to painful stimuli.
For example, adaptation happens when your eyes adjust from a dark movie theatre during a matinee to the bright sunlight outside. Whether pain receptors truly adapt or rescale their responses (versus simply desensitising) has been an open question.
Scientists had previously linked the analgesic or pain-relieving effects of capsaicin to a lipid called PIP2, found in cell membranes. When capsaicin is applied to the skin it induces a strong depletion of PIP2 in the cell membrane.
"The receptor acts like a gate to the neurons," said Qin. "When stimulated it opens, letting outside calcium enter the cells until the receptor shuts down, a process called desensitisation."
"The analgesic action of capsaicin is believed to involve this desensitization process. However, how the entry of calcium leads to the loss of sensitivity of the neurons was not clear," he said, according to a Buffalo release.
Capsaicin creams are commonly sold over the counter as effective treatment for a variety of pain syndromes, from minor muscle or joint aches to those that are very difficult to treat, such as arthritis and neuropathic pain.
These findings were published this week's edition of PLoS Biology.