Rabbit Anti-Human PKM2 Polyclonal Antibody Knockout Validated

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

Chronic inflammatory pain can induce emotional diseases. Electroacupuncture (EA) has effects on chronic pain and pain-related anxiety. Protein kinase Mzeta (PKMzeta) has been proposed to be essential for the maintenance of pain and may interact with GluR1 to maintain CNS plasticity in the anterior cingulate cortex (ACC). We hypothesized that the PKMzeta-GluR1 pathway in the ACC may be involved in anxiety-like behaviors of chronic inflammatory pain and that the mechanism of EA regulation of pain emotion may involve the PKMzeta pathway in the ACC. Our results showed that chronic inflammatory pain model decreased the paw withdrawal threshold (PWT) and increased anxiety-like behaviors. The protein expression of PKCzeta, p-PKCzeta (T560), PKMzeta, p-PKMzeta (T560), and GluR1 in the ACC of the model group were remarkably enhanced. EA increased PWT and alleviated anxiety-like behaviors. EA significantly inhibited the protein expression of p-PKMzeta (T560) in the ACC, and only a downward trend effect for other substances. Further, the microinjection of ZIP remarkably reversed PWT and anxiety-like behaviors. The present study provides direct evidence that the PKCzeta/PKMzeta-GluR1 pathway is related to pain and pain-induced anxiety-like behaviors. EA treatment both increases pain-related somatosensory behavior and decreases pain-induced anxiety-like behaviors by suppressing PKMzeta activity in the ACC.