The Mechanisms Of RSNSR1 On CFA-evoked Inflammatory Pain

Nitro oxide (NO),c-Fos protein and endogenous opioid peptide are present in the nervous system and involved in the pathological process of inflammatory pain. It has been demonstrated that rSNSR1 alleviates CFA-evoked inflammatory pain. The present study was designed to investigate the mechanisms of the analgesia effect of intrathecal activation of rSNSR1 on CFA-evoked inflammatory pain.This study was conducted by using behavioral,immunohistochemical and Western blot techniques. We found that: intrathecal injection of CTAP, inhibited the analgesia effect of intrathecal activation of rSNSR1 on CFA-evoked inflammatory pain; intrathecal activation of rSNSR1 produced an decrease in the expression of nruronal nitric oxide synthase(nNOS),and c-fos protein in the spinal cord dorsal horn, but P-endorphin is not changed in DRG and inflamed tissue.This study shows that the mechanisms of the analgesia effect of intrathecal activation of rSNSR1 on CFA-evoked inflammatory pain may be related to endogenous opioid peptide,NO and c-Fos signaling pathways, but if related toβ-EP signaling pathway has to be researched more.