Changes in the expression of voltage-gated sodium channels Nav1.3, Nav1.7, Nav1.8, and Nav1.9 in rat trigeminal ganglia following chronic constriction injury
Changes in the expression of voltage-gated sodium channels Nav1.3, Nav1.7, Nav1.8, and Nav1.9 in rat trigeminal ganglia following chronic constriction injury
复制标题
慢性缩窄性损伤后大鼠三叉神经节电压门控钠通道Nav1.3、Nav1.7、Nav1.8和Nav1.9表达的变化
DOI：
10.1097/wnr.0000000000000632
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发表时间：
2016-08-17
期刊：
影响因子：
1.7
通讯作者：
Wang, Xuxia
中科院分区：
文献类型：
--
作者：
Xu, Wenhua;Zhang, Jun;Wang, Xuxia
Voltage-gated sodium channels (VGSCs), especially the tetrodotoxin-sensitive Nav1.3 and Nav1.7, and the tetrodotoxin-resistant Nav1.8 and Nav1.9, have been implicated in acute and chronic neuropathic pain. The aim of this study was to investigate the expression of VGSC Nav1.3, Nav1.7, Nav1.8, and Nav1.9 after nerve injury and their roles in the development of trigeminal neuralgia (TN). We used the infraorbital nerve-chronic constriction injury model of TN in the rat. The time course of changes in the mechanical pain threshold was examined. In addition, real-time PCR and double immunofluorescence staining of VGSC &agr; subunits were used to evaluate messenger RNA and protein expression, respectively, in the trigeminal ganglion. Behavioral tests showed that the mechanical pain threshold decreased significantly 4–42 days after surgery and reached the lowest observed value by day 12. Compared with sham-operated controls, we found that trigeminal ganglion in rats subjected to an infraorbital nerve-chronic constriction injury showed upregulation of Nav1.3 and downregulation of Nav1.7, Nav1.8, and Nav1.9 messenger RNA and protein levels. Our findings suggest that VGSC may participate in the regulation of TN.
