Prostaglandin E2 (PGE2) is one of the inflammatory mediators that play important roles in pain sensation and hyperalgesia in inflamed tissues by exciting or sensitizing nociceptors, and inhibition of PGE2 production by cyclooxygenase blockers is a popular way to treat pain and inflammation. The capsaicin receptor TRPV1 is a nonselective cation channel exclusively expressed in sensory neurons and activated by various stimuli known to cause nociception in vivo such as capsaicin, protons, heat and some lipids. We examined the interaction between TRPV1 and PGE2. In behavioral analysis, intraplantar injection of PGE2 produced thermal hyperalgesia in wild type mice. However PGE2-induced thermal hyperalgesia completely abolished in TRPV1-deficient mice. PGE2-induced potentiation of capsaicin-activated current responses was observed in mouse dorsal root ganglion neurons. These data suggest that TRPV1 is necessary for the development of PGE2-induced thermal hyperalgesia in vivo. [Jpn J Physiol 54 Suppl:S169 (2004)]
