【Objective】To observe the expression of PKCε and μ opioid receptor（MOR）and explore their relationship in the spinal cord of rats with remifentanil-induced hyperalgesia（RIH）.【Methods】Eighteenadult male SD rats were randomly divided into control group ，saline group and remifentanil group with 6 rats in each group. Hyperalgesia was induced by continuous infusion of 4 μg（/   kg·min）remifentanil for 2 hours via vein tail. Pain sensitivity was assessed by the Hargreaves test to determine paw withdrawl latency to a thermal stimulus at 6 h and 24 h after remifentanil administration. Real- time fluorescent quantitative PCR and Western blot analysis were used to measure the expression levels of PKC ε and MOR in the spinal cord of rats and their distribution was detected by immunofluorescence. In order to observe the effect of inhibitors on RIH and the protein expression of MOR in the spinal cord of rats，we injected different PKC inhibitors including Bisindolylmaleimide I（BIS，inhibiting PKCε）and Gö6983（not inhibiting PKCε）intrathecally 30 mins prior to remifentanil infusion.【Results】The results of behavioral experiment showed that the paw withdrawal thermal latency was significantly reduced at 24 h after remifentanil infusion［PWTL=（5.31 ± 0.87）s，P < 0.01］. Western blot and Real time PCR results revealed upregulated PKCε expression（P<0.001）and downregulated MOR expression（P<0.001）. Immunofluorescence results indicated that PKCε and MOR were colocalized with neurons in the dorsal horn of rat spinal cord. Preemptive intrathecal injection of BIS alleviated the hyperalgesia in rats and inhibited MOR expression（P<0.001），but injection of Gö6983made no difference（P>0.05）.【Conclusion】PKC ε and MORin spinal dorsal horn neurons may be involved in RIH，and PKCε may regulate the expression levels of MOR. This research provides a new theoretical mechanism for the prevention and treatment of RIH.