Previous studies have shown that protein kinase M zeta (PKMζ), a brain-specific isoform of protein kinase C, is involved in the central processing of nociception in several pain models by using a synthetic zeta inhibitory peptide. In the present study, we investigated whether PKMζ contributes to the pathogenesis of postsurgical pain using both conditional and conventional PKMζ knockout mice. Our results showed that the expression of PKMζ in anterior cingulate cortex, but not spinal cord, of the conditional PKMζ knockout mice was inhibited following tamoxifen injection. And the conditional PKMζ knockout mice displayed similar plantar incision-produced postsurgical pain responses as those in wild-type mice. Moreover, the expression of PKMζ was inhibited in both anterior cingulate cortex and spinal cord of the conventional PKMζ knockout mice. And there were no significant differences in the development of postsurgical pain among wild-type, heterozygous, and homozygous conventional PKMζ knockout mice. These data suggest that PKMζ is not required for the development of postsurgical pain after plantar incision.
Keywords: Anterior cingulate cortex; PKMζ; Plantar incision; Postsurgical pain; Spinal cord; Synaptic plasticity.