Syndecan-3 (SDC3) and Syndecan-4 (SDC4) are distributed throughout the nervous system (NS) and are favourable factors in motor neuron development. They are also essential for regulation of neurite outgrowth in the CNS. However, their roles in the reconstruction of the nodes of Ranvier after peripheral nerve injury (PNI) are still unclear. Present study used an in vivo model of end-to-side neurorrhaphy (ESN) for 1–3 months. The recovery of neuromuscular function was evaluated by grooming test. Expression and co-localization of SDC3, SDC4, and Nav1.6 channel (Nav1.6) at regenerating axons were detected by proximity ligation assay and confocal microscopy after ESN. Time-of-flight secondary ion mass spectrometry was used for imaging ions distribution on tissue. Our data showed that the re-clustering of sodium and Nav1.6 at nodal regions of the regenerating nerve corresponded to the distribution of SDC3 after ESN. Furthermore, the re-establishment of sodium and Nav1.6 correlated with the recovery of muscle power 3 months after ESN. This study suggested syndecans may involve in stabilizing Nav1.6 and further modulate the distribution of sodium at nodal regions after remyelination. The efficiency of sodium re-clustering was improved by the assistance of anionic syndecan, resulting in a better functional repair of PNI.

Syndecan-3 (SDC3) 和 Syndecan-4 (SDC4) 分布于整个神经系统 (NS)，是运动神经元发育的有利因素。它们对于调节 CNS 中的神经突生长也是必不可少的。然而，它们在周围神经损伤 (PNI) 后 Ranvier 节点重建中的作用仍不清楚。本研究使用了 1-3 个月的端对侧神经损伤 (ESN) 体内模型。通过理毛试验评价神经肌肉功能的恢复情况。在 ESN 后通过邻近连接测定和共聚焦显微镜检测 SDC3、SDC4 和 Nav1.6 通道 (Nav1.6) 在再生轴突的表达和共定位。飞行时间二次离子质谱法用于成像组织上的离子分布。我们的数据显示钠和 Nav1. 6 在再生神经的节点区域对应于 ESN 后 SDC3 的分布。此外，钠和 Nav1.6 的重建与 ESN 后 3 个月肌肉力量的恢复相关。该研究表明，syndecans 可能参与稳定 Nav1.6 并进一步调节髓鞘再生后节点区域的钠分布。阴离子合成聚糖的辅助提高了钠离子重聚的效率，从而更好地修复了 PNI 的功能。