Hyperalgesic priming (type II) induced by repeated opioid exposure: maintenance mechanisms.

摘要: We previously developed a model of opioid-induced neuroplasticity in the peripheral terminal nociceptor that could contribute to hyperalgesia, type II hyperalgesic priming. Repeated administration mu-opioid receptor (MOR) agonists, such as DAMGO, at nociceptor, induces long-lasting plasticity expressed, prototypically hyperalgesia and prolongation prostaglandin E2-induced hyperalgesia. In this study, we evaluated mechanisms involved maintenance Opioid antagonist, naloxone, induced DAMGO-primed paws. When repeatedly injected, naloxone-induced priming, supporting suggestion priming involves changes MOR signaling. However, knockdown with oligodeoxynucleotide antisense did not reverse Mitogen-activated protein kinase focal adhesion kinase, which are Src signaling pathway, implicated also inhibited expression, but when mitogen-activated inhibitors were coadministered, was reversed, male rats. A second latent sensitization, by complete Freund's adjuvant males. females, inhibitor combination only able inhibit expression DAMGO-induced G-protein-coupled estrogen 30 (GPR30) performed. These findings demonstrate sensitization is mediated an interaction between, MAP kinases, females GPR30 dependent.