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Cell Rep. 2018 Jan 16;22(3):748-759. doi: 10.1016/j.celrep.2017.12.059.

Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury.

Author information

1
School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea; Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
2
School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea.
3
Max Planck Institute of Psychiatry, Department of Translational Research in Psychiatry, Kraepelinstr. 2, 80804 Munich, Germany.
4
Department of Dental Anesthesiology and Dental Research Institute, School of Dentistry, Seoul National University, Seoul 03080, South Korea.
5
Centre for Synaptic Plasticity, School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol BS8 1TD, UK; Department of Physiology, Faculty of Medicine, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada; Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON M5G 1X5, Canada. Electronic address: g.collingridge@utoronto.ca.
6
Department of Physiology, Faculty of Medicine, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada; Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: min.zhuo@utoronto.ca.
7
School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea; Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: kaang@snu.ac.kr.

Abstract

Peripheral nerve injury can induce pathological conditions that lead to persistent sensitized nociception. Although there is evidence that plastic changes in the cortex contribute to this process, the underlying molecular mechanisms are unclear. Here, we find that activation of the anterior cingulate cortex (ACC) induced by peripheral nerve injury increases the turnover of specific synaptic proteins in a persistent manner. We demonstrate that neural cell adhesion molecule 1 (NCAM1) is one of the molecules involved and show that it mediates spine reorganization and contributes to the behavioral sensitization. We show striking parallels in the underlying mechanism with the maintenance of NMDA-receptor- and protein-synthesis-dependent long-term potentiation (LTP) in the ACC. Our results, therefore, demonstrate a synaptic mechanism for cortical reorganization and suggest potential avenues for neuropathic pain treatment.

KEYWORDS:

NCAM1; neural cell adhesion molecule 1; neuropathic pain; protein turnover; synaptic reorganization

PMID:
29346771
DOI:
10.1016/j.celrep.2017.12.059
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