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Mol Pain. 2018 Jan-Dec;14:1744806918783943. doi: 10.1177/1744806918783943.

Transcription-independent expression of PKMζ in the anterior cingulate cortex contributes to chronically maintained neuropathic pain.

Author information

1
1 School of Biological Sciences, Seoul National University, Seoul, Republic of Korea.
2
2 Department of Pharmacology, Wonkwang University School of Medicine, Iksan, Republic of Korea.
3
3 Department of Anatomy, Graduate School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
4
4 Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
5
5 Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, China.

Abstract

Protein 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.

KEYWORDS:

Protein kinase M ζ; anterior cingulate cortex; chronic pain; neuropathic pain

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