郎飞结作为屏障，限制有髓轴突中侧翼结旁区域的入侵。
Nodes of Ranvier act as barriers to restrict invasion of flanking paranodal domains in myelinated axons.
作者信息
Thaxton Courtney, Pillai Anilkumar M, Pribisko Alaine L, Dupree Jeffrey L, Bhat Manzoor A
机构信息
Department of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, Chapel Hill, NC 27599-7545, USA.
出版信息
Neuron. 2011 Jan 27;69(2):244-57. doi: 10.1016/j.neuron.2010.12.016.
Accumulation of voltage-gated sodium (Na(v)) channels at nodes of Ranvier is paramount for action potential propagation along myelinated fibers, yet the mechanisms governing nodal development, organization, and stabilization remain unresolved. Here, we report that genetic ablation of the neuron-specific isoform of Neurofascin (Nfasc(NF¹⁸⁶)) in vivo results in nodal disorganization, including loss of Na(v) channel and ankyrin-G (AnkG) enrichment at nodes in the peripheral nervous system (PNS) and central nervous system (CNS). Interestingly, the presence of paranodal domains failed to rescue nodal organization in the PNS and the CNS. Most importantly, using ultrastructural analysis, we demonstrate that the paranodal domains invade the nodal space in Nfasc(NF¹⁸⁶) mutant axons and occlude node formation. Our results suggest that Nfasc(NF¹⁸⁶)-dependent assembly of the nodal complex acts as a molecular boundary to restrict the movement of flanking paranodal domains into the nodal area, thereby facilitating the stereotypic axonal domain organization and saltatory conduction along myelinated axons.
电压门控性钠（Na(v)）通道在郎飞结处的聚集对于动作电位沿有髓纤维的传播至关重要，然而，调控结发育、组织和稳定的机制仍未明确。在此，我们报道，体内神经元特异性神经束蛋白异构体（Nfasc(NF¹⁸⁶)）的基因敲除导致结紊乱，包括外周神经系统（PNS）和中枢神经系统（CNS）中结处Na(v)通道和锚蛋白-G（AnkG）富集的丧失。有趣的是，旁结结构域的存在未能挽救PNS和CNS中的结组织。最重要的是，通过超微结构分析，我们证明旁结结构域侵入Nfasc(NF¹⁸⁶)突变轴突的结间隙并阻碍结的形成。我们的结果表明，依赖Nfasc(NF¹⁸⁶)的结复合体组装作为分子边界，限制侧翼旁结结构域向结区域的移动，从而促进有髓轴突上刻板的轴突结构域组织和跳跃传导。
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