PKM Is Not Required for Development of Postsurgical Pain.
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Previous studies have shown that protein kinase M zeta (PKM), 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 PKM contributes to the pathogenesis of postsurgical pain using both conditional and conventional PKM knockout mice. Our results showed that the expression of PKM in anterior cingulate cortex, but not spinal cord, of the conditional PKM knockout mice was inhibited following tamoxifen injection. And the conditional PKM knockout mice displayed similar plantar incision-produced postsurgical pain responses as those in wild-type mice. Moreover, the expression of PKM was inhibited in both anterior cingulate cortex and spinal cord of the conventional PKM knockout mice. And there were no significant differences in the development of postsurgical pain among wild-type, heterozygous, and homozygous conventional PKM knockout mice. These data suggest that PKM is not required for the development of postsurgical pain after plantar incision.