Cell Reports (Jan 2018)
Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury
- Hyoung-Gon Ko,
- Jun-Hyeok Choi,
- Dong Ik Park,
- SukJae Joshua Kang,
- Chae-Seok Lim,
- Su-Eon Sim,
- Jaehoon Shim,
- Ji-Il Kim,
- Siyong Kim,
- Tae-Hyeok Choi,
- Sanghyun Ye,
- Jaehyun Lee,
- Pojeong Park,
- Somi Kim,
- Jeehaeh Do,
- Jihye Park,
- Md Ariful Islam,
- Hyun Jeong Kim,
- Christoph W. Turck,
- Graham L. Collingridge,
- Min Zhuo,
- Bong-Kiun Kaang
Affiliations
- Hyoung-Gon Ko
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Jun-Hyeok Choi
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Dong Ik Park
- Max Planck Institute of Psychiatry, Department of Translational Research in Psychiatry, Kraepelinstr. 2, 80804 Munich, Germany
- SukJae Joshua Kang
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Chae-Seok Lim
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Su-Eon Sim
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Jaehoon Shim
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Ji-Il Kim
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Siyong Kim
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Tae-Hyeok Choi
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Sanghyun Ye
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Jaehyun Lee
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Pojeong Park
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Somi Kim
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Jeehaeh Do
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Jihye Park
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Md Ariful Islam
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- Hyun Jeong Kim
- Department of Dental Anesthesiology and Dental Research Institute, School of Dentistry, Seoul National University, Seoul 03080, South Korea
- Christoph W. Turck
- Max Planck Institute of Psychiatry, Department of Translational Research in Psychiatry, Kraepelinstr. 2, 80804 Munich, Germany
- Graham L. Collingridge
- Centre for Synaptic Plasticity, School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol BS8 1TD, UK
- Min Zhuo
- Department of Physiology, Faculty of Medicine, University of Toronto, 1 King’s College Circle, Toronto, ON M5S 1A8, Canada
- Bong-Kiun Kaang
- School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea
- DOI
- https://doi.org/10.1016/j.celrep.2017.12.059
- Journal volume & issue
-
Vol. 22,
no. 3
pp. 748 – 759
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
