• Hyoung-Gon Ko, Sanghyun Ye, Dae-Hee Han, Pojeong Park, Chae-Seok Lim, Kyungmin Lee, Min Zhuo, and Bong-Kiun Kaang.
• 1 School of Biological Sciences, Seoul National University, Seoul, Republic of Korea.
• Mol Pain. 2018 Jan 1; 14: 1744806918783943.

AbstractProtein kinase M ζ is well known for its role in maintaining memory and pain. Previously, we revealed that the activation of protein kinase M ζ in the anterior cingulate cortex plays a role in sustaining neuropathic pain. However, the mechanism by which protein kinase M ζ is expressed in the anterior cingulate cortex by peripheral nerve injury, and whether blocking of protein kinase M ζ using its inhibitor, zeta inhibitory peptide, produces analgesic effects in neuropathic pain maintained chronically after injury, have not previously been resolved. In this study, we show that protein kinase M ζ expression in the anterior cingulate cortex is enhanced by peripheral nerve injury in a transcription-independent manner. We also reveal that the inhibition of protein kinase M ζ through zeta inhibitory peptide treatment is enough to reduce mechanical allodynia responses in mice with one-month-old nerve injuries. However, the zeta inhibitory peptide treatment was only effective for a limited time.

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