Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury
| Autor: | Christoph W. Turck, Somi Kim, Hyun Jeong Kim, Ji-il Kim, Jaehoon Shim, Sanghyun Ye, Hyoung-Gon Ko, Siyong Kim, Jeehaeh Do, Ariful Islam, Sukjae Joshua Kang, Jihye Park, Su-Eon Sim, Chae-Seok Lim, Min Zhuo, Jaehyun Lee, Dong Ik Park, Graham L. Collingridge, Jun-Hyeok Choi, Pojeong Park, Tae-Hyeok Choi, Bong-Kiun Kaang |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Dendritic spine synaptic reorganization Gyrus Cinguli Synaptic Transmission General Biochemistry Genetics and Molecular Biology Mice 03 medical and health sciences 0302 clinical medicine Peripheral Nerve Injuries Cortex (anatomy) medicine Animals lcsh:QH301-705.5 Anterior cingulate cortex NCAM1 neuropathic pain Chemistry protein turnover Long-term potentiation CD56 Antigen 030104 developmental biology Nociception medicine.anatomical_structure lcsh:Biology (General) neural cell adhesion molecule 1 Synapses Peripheral nerve injury Neural cell adhesion molecule Memory consolidation Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Ko, H-G, Choi, J-H, Park, D I, Kang, S J, Lim, C-S, Sim, S-E, Shim, J, Kim, J-I, Kim, S, Choi, T-H, Ye, S, Lee, J, Park, P, Kim, S, Do, J, Park, J, Islam, M A, Kim, H J, Turck, C W, Collingridge, G L, Zhuo, M & Kaang, B-K 2018, ' Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury ', Cell Reports, vol. 22, no. 3, pp. 748-759 . https://doi.org/10.1016/j.celrep.2017.12.059 CELL REPORTS Cell Reports, Vol 22, Iss 3, Pp 748-759 (2018) |
| ISSN: | 2211-1247 |
| DOI: | 10.1016/j.celrep.2017.12.059 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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