Abstract
We have previously demonstrated that peripheral administration of 15d-PGJ2 in the Temporomandibular joint (TMJ) of rats can prevent nociceptor sensitization, mediated by peroxisome proliferator activated receptor-γ (PPAR-γ), and κ- and δ- opioid receptors. However, the mechanism that underlies the signaling of PPAR-γ (upon activation by 15d-PGJ2) to induce antinociception, and how the opioid receptors are activated via 15d-PGJ2 are not fully understood. This study demonstrates that peripheral antinociceptive effect of 15d-PGJ2 is mediated by PPAR-γ expressed in the inflammatory cells of TMJ tissues. Once activated by 15d-PGJ2, PPAR-γ induces the release of β-endorphin and dynorphin, which activates κ- and δ-opioid receptors in primary sensory neurons to induce the antinociceptive effect.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
