Sodium channel Nav1.6 accumulates at the site of infraorbital nerve injury.
Sodium channel Nav1.6 accumulates at the site of infraorbital nerve injury.
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DOI：
10.1186/1471-2202-8-56
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发表时间：
2007-07-27
期刊：
影响因子：
2.4
通讯作者：
Levinson SR
中科院分区：
文献类型：
--
作者：
Henry MA;Freking AR;Johnson LR;Levinson SR
钠通道（NaCh）的表达在神经和炎症损伤后发生变化，这种变化可能有助于激活疼痛通路。在以前的研究中，我们发现了一个显着增加的大小和密度的氯化钠积累，和重塑氯化钠在完整的和改变的有髓鞘的网站在一个位置的组合部分轴突切断和铬缝合病变的大鼠眶下神经（ION）与使用的抗体，确定所有氯化钠亚型。在这里，我们评估的贡献，主要的节点NaCh亚型，Nav1.6，这种重塑NaCh以下相同的病变。将来自正常和ION病变受试者的ION切片用针对Nav1.6和Caspr（接触素相关蛋白;识别Ranvier节点的旁结蛋白）的抗体双重染色，然后用共聚焦显微镜捕获z系列光学切片图像。使用ImageJ（NIH）软件来量化Nav1.6积聚的平均大小和密度，而另外的单纤维分析测量结间隙的轴向长度、结中Nav1.6的免疫荧光强度和结旁区域中的Caspr的免疫荧光强度。研究结果显示，与正常离子相比，受损离子中Nav1.6积聚的平均大小和密度显着增加。在caspr确定的典型节点的单纤维分析的结果表明，增加的轴向长度的节点间隙，增加免疫荧光强度的nodal Nav1.6和降低免疫荧光强度的paranodal半胱氨酸蛋白酶在病变的离子相比，正常的离子。在病变的离子，Nav1.6积累也被视为与改变caspr关系，如heminodes。本研究的结果确定Nav1.6作为一种亚型参与的增加和重塑的NaChs在节点的网站后，结合部分轴突切断和铬缝合ION病变。Nav1.6的增强可能是由于轴突-许旺细胞信号传导机制的改变，如Caspr表达的变化所示。本研究中确定的变化表明，在检查神经病理性疼痛模型中有髓鞘轴突兴奋性的变化时，应考虑Nav1.6的参与。
Sodium channel (NaCh) expressions change following nerve and inflammatory lesions and this change may contribute to the activation of pain pathways. In a previous study we found a dramatic increase in the size and density of NaCh accumulations, and a remodeling of NaChs at intact and altered myelinated sites at a location just proximal to a combined partial axotomy and chromic suture lesion of the rat infraorbital nerve (ION) with the use of an antibody that identifies all NaCh isoforms. Here we evaluate the contribution of the major nodal NaCh isoform, Nav1.6, to this remodeling of NaChs following the same lesion. Sections of the ION from normal and ION lesioned subjects were double-stained with antibodies against Nav1.6 and caspr (contactin-associated protein; a paranodal protein to identify nodes of Ranvier) and then z-series of optically sectioned images were captured with a confocal microscope. ImageJ (NIH) software was used to quantify the average size and density of Nav1.6 accumulations, while additional single fiber analyses measured the axial length of the nodal gap, and the immunofluorescence intensity of Nav1.6 in nodes and of caspr in the paranodal region. The findings showed a significant increase in the average size and density of Nav1.6 accumulations in lesioned IONs when compared to normal IONs. The results of the single fiber analyses in caspr-identified typical nodes showed an increased axial length of the nodal gap, an increased immunofluorescence intensity of nodal Nav1.6 and a decreased immunofluorescence intensity of paranodal caspr in lesioned IONs when compared to normal IONs. In the lesioned IONs, Nav1.6 accumulations were also seen in association with altered caspr-relationships, such as heminodes. The results of the present study identify Nav1.6 as one isoform involved in the augmentation and remodeling of NaChs at nodal sites following a combined partial axotomy and chromic suture ION lesion. The augmentation of Nav1.6 may result from an alteration in axon-Schwann cell signaling mechanisms as suggested by changes in caspr expression. The changes identified in this study suggest that the participation of Nav1.6 should be considered when examining changes in the excitability of myelinated axons in neuropathic pain models.
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影响因子：
4
作者：
Devor, M
通讯作者：
Devor, M
影响因子：
7.4
作者：
Henry, Michael A.;Freking, Angelique R.;Levinson, S. Rock
通讯作者：
Levinson, S. Rock
影响因子：
5.3
作者：
Rios, JC;Rubin, M;Salzer, JL
通讯作者：
Salzer, JL
DOI：
10.1073/pnas.87.17.6777
发表时间：
1990-09-01
影响因子：
11.1
作者：
ENGLAND, JD;GAMBONI, F;FINGER, TE
通讯作者：
FINGER, TE
影响因子：
16.2
作者：
Poliak, S;Gollan, L;Peles, E
通讯作者：
Peles, E