Effects of N-methyl-D-aspartate receptor on remifentanil-induced hyperalgesia

Opioids especially remifentanil have been widely used in clinical operation as inducer for general anesthesia and could cause hyperalgesia. N-methyl and D-aspartate-related receptor (NMDAR) is widely found in animal and plays an important role in central nerve system and hypersensitivity. Our study aimed to investigate the molecular mechanism of N-methyl-D-aspartate receptor on remifentanil-induced hyperalgesia in rat model. A rat model of remifentanil-induced hyperalgesia for intravenous injection was established. Spinal cord of hyperalgesia rat was used to perform PRT-PCR and western blot to detect the expression of NMDAR, PKC and phosphorylate PKC. After intravenous infusion of PKC inhibitor Staurosporine into hyperalgesia rat, algesia time of rat, expression of NMDAR and PKC, as well as activation of PKC were examined to investigate the role of PKC signal pathway on expression of NMDAR and remifentanil-induced hyperalgesia of rat. The expression of NMDAR and PKC in spinal cord of hyperalgesia rat induced by remifentanil was increased. Compared to control group, there was significant difference on the activation of PKC (P<0.05). Intravenously injection of PKC inhibitor Staurosporine was obviously inhibit the algesia time induced by remifentanil (P<0.05), and the expresssion of NMDAR and PKC were reduced and activation of PKC was inhibited. N-methyl-D-aspartate receptor played an important role in remifentanil-induced hyperalgesia through PKC signal pathway.