TNF-α contributes to up-regulation of Nav1.3 and Nav1.8 in DRG neurons following motor fiber injury

背根神经节 钠通道 神经损伤 导航1 坐骨神经 轴突切开术 神经病理性疼痛 周围神经损伤 神经科学 伤害 坐骨神经损伤 医学 化学 受体 内科学 生物 感觉系统 中枢神经系统 有机化学
作者
Xin-Hua He,Ying Zang,Xi Chen,Rui‐Ping Pang,Ji‐Tian Xu,Xiang Zhou,Xu‐Hong Wei,Yongyong Li,Wen‐Jun Xin,Zhihai Qin,Xian‐Guo Liu
出处
期刊:Pain [Ovid Technologies (Wolters Kluwer)]
卷期号:151 (2): 266-279 被引量:153
标识
DOI:10.1016/j.pain.2010.06.005
摘要

A large body of evidence has demonstrated that the ectopic discharges of action potentials in primary afferents, resulted from the abnormal expression of voltage gated sodium channels (VGSCs) in dorsal root ganglion (DRG) neurons following peripheral nerve injury are important for the development of neuropathic pain. However, how nerve injury affects the expression of VGSCs is largely unknown. Here, we reported that selective injury of motor fibers by L5 ventral root transection (L5-VRT) up-regulated Nav1.3 and Nav1.8 at both mRNA and protein level and increased current densities of TTX-S and TTX-R channels in DRG neurons, suggesting that nerve injury may up-regulate functional VGSCs in sensory neurons indirectly. As the up-regulated Nav1.3 and Nav1.8 were highly co-localized with TNF-α, we tested the hypothesis that the increased TNF-α may lead to over-expression of the sodium channels. Indeed, we found that peri-sciatic administration of recombinant rat TNF-α (rrTNF) without any nerve injury, which produced lasting mechanical allodynia, also up-regulated Nav1.3 and Nav1.8 in DRG neurons in vivo and that rrTNF enhanced the expression of Nav1.3 and Nav1.8 in cultured adult rat DRG neurons in a dose-dependent manner. Furthermore, inhibition of TNF-α synthesis, which prevented neuropathic pain, strongly inhibited the up-regulation of Nav1.3 and Nav1.8. The up-regulation of the both channels following L5-VRT was significantly lower in TNF receptor 1 knockout mice than that in wild type mice. These data suggest that increased TNF-α may be responsible for up-regulation of Nav1.3 and Nav1.8 in uninjured DRG neurons following nerve injury.
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