Specific translocation of protein kinase Cγ to lipid rafts in primary somatosensory cortex is involved in remifentanil-induced hyperalgesia

Abstract

Objective To determine the involvement of neuron-specific protein kinase C γ isoform(PKCγ) translocation to lipid rafts in primary somatosensory cortex(S1) in remifentanil-induced hyperalgesia. Methods Fifty adult male SD rats weighing 240-260 g (at the age of 8-10 weeks) were randomly assigned to 3 groups: control, the propofol (group P) and the remifentanil group (group R). Intravenous anesthesia with either propofol (group P) or propofol combined with remifentanil(group R) was performed through a 24 G catheter inserted in tail vein for 3 h. The total doses of propofol were 36.0 mg and 26.0 mg in group P and R, respectively. The dose of remifentanil was 19.5 g in group R. Mechanical allodynia in the rats was evaluated by the von Frey filament test, and PKCγ levels in the whole-cell lysates and lipid rafts in the S1 neurons were determined by Western blot. Results ① The threshold of paw-withdrawal response to von Frey filament stimulation in group R at 2 h after stopping drug infusion was significantly lower than that in group P(P<0.05). ② Two hours after stopping drug infusion, the PKCγ protein levels in the lipid rafts of S1 in group R were significantly higher than those in group R(P<0.05). Conclusions These results suggest that increased translocation of PKCγ to lipid raft of S1 neurons may contribute to postoperative pain in rats after propofol-remifentanil-based anesthesia. Key words: Remifentanil; Hyperalgesia; Protein kinase C γisoform; Lipid rafts; Primary somatosensory cortex