Abstract: Objective To determine the involvement of conventional protein kinase Cgamma (cPKCγ) in the inhibitory action of lidocaine on remifentanil-induced hyperalgesia of rats after propofol-remifentanil-based anesthesia. Method Male Sprague-Dawley rats were allocated into the following groups randomly: propofol only (Group P), propofol+remifentanil (Group R), propofol+remifentanil+lidocaine (Group RL), and propofol+lidocaine (Group L). Cumulative pain score and withdrawal response to mechanical stimulation, immunoblotting, and immunofluorescence were applied to observe remifentanil-induced hyperalgesia and cPKCγ membrane translocation. Result 1) Cumulative pain score in Group R were higher than the other groups on postanesthesia 120min (P<0.05). While it were similar among Group P, RL and L. 2) Withdrawal threshold on the ipsilateral side to incised plantar in Group R were lower than the other groups (P<0.05) on posteanesthesia 120min. 3) Both immunoblotting and immunofluorescence demonstrated that the membrane translocation of PKCγ in dorsal horn neurons increased in propofol-remifentanil anesthetized animals and systemic lidocaine could inhibited it. Surgery procedure won’t affect the membrane translocation of PKCγ in dorsal horn neurons shortly after anesthesia. Conclusion Increased PKCγ membrane translocation in spinal dorsal horn involves in remifentanil-induced hyperalgesia, which was inhibited by systemic lidocaine and may contributes to reduced postoperative pain in rats after remifentanil-based anesthesia.