Alleviating Neuropathic Pain Hypersensitivity by Inhibiting PKMζ in the Anterior Cingulate Cortex-Reference-Cited by-同舟云学术

Alleviating Neuropathic Pain Hypersensitivity by Inhibiting PKMζ in the Anterior Cingulate Cortex

Published:2010-12-03 Issue:6009 Volume:330 Page:1400-1404
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Li Xiang-Yao¹²,Ko Hyoung-Gon³,Chen Tao¹²,Descalzi Giannina¹,Koga Kohei¹,Wang Hansen¹,Kim Susan S.¹,Shang Yuze¹,Kwak Chuljung³,Park Soo-Won³,Shim Jaehoon²³,Lee Kyungmin³⁴,Collingridge Graham L.²⁵,Kaang Bong-Kiun²³,Zhuo Min¹²

Affiliation:

1. Department of Physiology, Faculty of Medicine, Center for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.

2. Department of Brain and Cognitive Sciences, Seoul National University, Seoul 151 747, Korea.

3. National Creative Research Initiative Center for Memory, Department of Biological Sciences, College of Natural Sciences, Seoul National University, San 56-1 Silim-dong, Gwanak-gu, Seoul 151-747, Korea.

4. Department of Anatomy, School of Medicine, Kyungpook National University, 2-101 Dongin-Dong, Daegu 700-422, Korea.

5. Medical Research Council (MRC) Centre for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK.

Abstract

Pain in the Brain One of the major challenges in pain research is finding ways to reverse chronic pain. Synaptic long-term potentiation (LTP) at spinal or cortical levels is a cellular model of chronic pain. X.-Y. Li. et al. (p. 1400 ) studied the role of the enzyme protein kinase M zeta (PKMζ) in neurons of the anterior cingulate cortex (ACC) in the maintenance of LTP and for enhanced pain sensitivity after peripheral nerve injury in mice. Nerve injury appeared to lead to the up-regulation and phosphorylation of PKMζ. This triggered LTP at some synapses in the ACC by increasing the number of AMPA receptors. LTP was restricted to ACC neurons that were activated by nerve injury. Blocking PKMζ in the ACC days after nerve injury normalized pain behavior. Thus, PKMζ may represent a promising target for the treatment of chronic pain.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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