UC Davis research finds chili pepper receptor reacts differently to pain triggers

Researchers at the UC Davis School of Medicine have found that the TRPV1 receptor, which senses pain and is activated by capsaicin—the compound that makes chili peppers hot—does not respond uniformly to all stimuli, according to Newswise.

The study, led by the UC Davis Department of Physiology and Membrane Biology and published in the Proceedings of the National Academy of Sciences, reveals that different triggers place TRPV1 into distinct functional states rather than a single activated state, as previously thought.

TRPV1 is located on pain-sensing nerve cells and detects heat, tissue injury, inflammation, and chemical compounds including capsaicin. Its role in pain pathways without involving opioid signaling makes it a promising target for nonaddictive pain medicines.

However, blocking TRPV1 has been challenging due to its important function in regulating body temperature. The new findings suggest that different stimuli stabilize different open states of TRPV1, each with unique properties, which could lead to more precise pain treatments.

The researchers measured electrical currents through individual TRPV1 channels activated by various stimuli and found consistent differences in conductance levels, indicating the receptor opens in distinct ways depending on the trigger, according to both Newswise and miragenews.com.