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.
School of Biological Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul 08826, South Korea.
Cell Rep. 2018 Jan 16;22(3):748-759. doi: 10.1016/j.celrep.2017.12.059.
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.
外周神经损伤可诱导导致持续敏化痛觉的病理状态。尽管有证据表明皮质的可塑性变化对此过程有贡献，但潜在的分子机制尚不清楚。在这里，我们发现外周神经损伤引起的前扣带皮层（ACC）的激活以持续的方式增加特定突触蛋白的周转率。我们证明神经细胞黏附分子 1（NCAM1）是涉及的分子之一，并表明它介导了脊柱重组并有助于行为敏化。我们在 ACC 中 NMDA 受体和蛋白质合成依赖性长时程增强（LTP）的维持的潜在机制中发现了惊人的相似之处。因此，我们的结果证明了皮质重组的突触机制，并为治疗神经性疼痛提供了潜在途径。
