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 CollingridgeMin Zhuo, Bong-Kiun Kaang

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

15 Citations (Scopus)
270 Downloads (Pure)


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.
Original languageEnglish
Pages (from-to)748-759
Number of pages12
JournalCell Reports
Issue number3
Publication statusPublished - 16 Jan 2018


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

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