【摘 要】
：
The over-expression of voltage gated sodium channels (VGSCs) in dorsal root ganglion (DRG) neurons contributes to neuropathic pain by generation of the ectopic discharges of action potentials.However,
【机 构】
：
Pain Reseach Center and Department of Physiology,Zhongshan Medical School of Sun Yat-Sen University,
【出 处】
：
International Conference for Physiological Sciences 2012(201
论文部分内容阅读
The over-expression of voltage gated sodium channels (VGSCs) in dorsal root ganglion (DRG) neurons contributes to neuropathic pain by generation of the ectopic discharges of action potentials.However, mechanisms of regulating VGSC expression are poorly understood.Our previous work has demonstrated that the proinflammatory cytokine TNF-α up-regulates VGSCs, in the present work we tested if anti-inflammatory cytokine IL-10 had opposite effect.Real-time PCR and western blotting revealed that the recombinant rat IL-10 (rrlL-10,200 pg/mL) down-regulated in both mRNA and protein levels in cultured DRG neurons.rrlL-10 also reversed the increase of Nav1.3 and Navl.8 expression induced by TNF-α.In consistent with the changes in mRNA and proteins of VGSCs, we found that rrlL-10 reduced the densities of TTX-sensitive and Nav1.8currents in control DRG neurons and in the neurons pretreated with recombinant rat TNF-α (rrTNF, 100 pg/mL) for 4 hours, in which sodium channels had been up-regulated, as revealed by patch-clamp recordings.These data suggested that IL-10might treat neuropathic pain by down-regulation of the sodium channels in DRG neurons.
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