We have previously demonstrated that peripheral administration of 15d-PGJ(2) in the Temporomandibular joint (TMJ) of rats can prevent nociceptor sensitization, mediated by peroxisome proliferator activated receptor-gamma (PPAR-gamma), and kappa- and delta- opioid receptors. However, the mechanism...

We have previously demonstrated that peripheral administration of 15d-PGJ(2) in the Temporomandibular joint (TMJ) of rats can prevent nociceptor sensitization, mediated by peroxisome proliferator activated receptor-gamma (PPAR-gamma), and kappa- and delta- opioid receptors. However, the mechanism that underlies the signaling of PPAR-gamma (upon activation by 15d-PGJ(2)) to induce antinociception, and how the opioid receptors are activated via 15d-PGJ(2) are not fully understood. This study demonstrates that peripheral antinociceptive effect of 15d-PGJ(2) is mediated by PPAR-gamma expressed in the inflammatory cells of TMJ tissues. Once activated by 15d-PGJ(2), PPAR-gamma induces the release of beta-endorphin and dynorphin, which activates kappa- and delta-opioid receptors in primary sensory neurons to induce the antinociceptive effect

CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQ

483988/2012

COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPES

FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP

2011/00683-5

fechado