Alleviating neuropathic pain hypersensitivity by inhibiting PKMzeta in the anterior cingulate cortex

XY Li, HG Ko, T Chen, G Descalzi, K Koga, H Wang, SS Kim, Y Shang, C Kwak, SW Park, J Shim, K Lee, GL Collingridge, BK Kaang, M Zhuo

Research output: Contribution to journalArticle (Academic Journal)peer-review

262 Citations (Scopus)

Abstract

Synaptic plasticity is a key mechanism for chronic pain. It occurs at different levels of the central nervous system, including spinal cord and cortex. Studies have mainly focused on signaling proteins that trigger these plastic changes, whereas few have addressed the maintenance of plastic changes related to chronic pain. We found that protein kinase M zeta (PKMζ) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC). Peripheral nerve injury caused activation of PKMζ in the ACC, and inhibiting PKMζ by a selective inhibitor, ζ-pseudosubstrate inhibitory peptide (ZIP), erased synaptic potentiation. Microinjection of ZIP into the ACC blocked behavioral sensitization. These results suggest that PKMζ in the ACC acts to maintain neuropathic pain. PKMζ could thus be a new therapeutic target for treating chronic pain.
Translated title of the contributionAlleviating neuropathic pain hypersensitivity by inhibiting PKMzeta in the anterior cingulate cortex
Original languageEnglish
Pages (from-to)1400 - 1404
Number of pages5
JournalScience
Volume330
Issue number6009
DOIs
Publication statusPublished - 3 Dec 2010

Bibliographical note

Publisher: American Association for the Advancement of Science

Fingerprint Dive into the research topics of 'Alleviating neuropathic pain hypersensitivity by inhibiting PKMzeta in the anterior cingulate cortex'. Together they form a unique fingerprint.

Cite this