成纤维细胞13因子作用于钠通道1.7选择性调控热痛

发布时间：2018-01-31 04:54

本文关键词： 热痛伤害性热刺激温度感受器钠通道成纤维细胞动作电位感觉神经元痛反应痛敏机械痛 　出处：《中国疼痛医学杂志》2017年04期 　论文类型：期刊论文

【摘要】：当前关于伤害性热痛的认识主要局限于温度感受器,如表达在背根神经节(DRG)伤害性感觉神经元上的瞬时受体电位阳离子通道(TRPV1)。但是温度感受器的缺失仅部分地影响热痛,表明热痛的产生和调控还存在未知机制。我们发现在小鼠DRG神经元中条件性敲除胞浆型成纤维细胞13因子(FGF),导致热痛选择性缺失;敲除了FGF13的DRG神经元,伤害性热刺激不能诱发动作电位的持续发放;FGF13与钠通道(Nav)1.7作用可以促进热痛的传导,增强伤害性热刺激诱发的Nav1.7电流并维持Nav1.7上膜过程,进而维持动作电位的持续发放。打破FGF13和Nav1.7相互作用抑制了热刺激诱发的动作电位和痛反射行为。因此,不同于温度感受器,FGF13和Nav1.7的相互作用对于维持热痛信号的产生和传递是至关重要的。
[Abstract]:Current knowledge of nociceptive heat pain is mainly confined to temperature receptors. For example, the transient receptor potential cationic channel (TRPV1) expressed in the nociceptive sensory neurons of DRG was only partially affected by the absence of thermosensitive receptors. We found that conditioned knockout of cytoplasmic fibroblast 13 factor 13 in mouse DRG neurons resulted in the absence of heat pain selectivity. If the DRG neurons of FGF13 were knocked out, nociceptive thermal stimulation could not induce the continuous release of action potential. The interaction of FGF13 with sodium channel Navine 1.7 can promote the conduction of thermal pain, enhance the Nav1.7 current induced by nociceptive heat stimulation and maintain the process of Nav1.7 supermembrane. Thus, breaking the interaction between FGF13 and Nav1.7 inhibits the action potential and pain reflex induced by thermal stimulation. Therefore, it is different from the temperature receptor. The interaction between FGF13 and Nav1.7 is essential to maintain the generation and transmission of thermal pain signals.
【分类号】：R402
【正文快照】： 研究背景 FGF分为外泌型和胞浆型,外泌型FGF在神经发育过程中发挥着重要作用,但对胞浆型FGF功能的研究却很少。FGF13是表达在神经系统中的胞浆型因子,在发育过程中的脑皮质神经元上有瞬时表达;在从发育早期到成年DRG中,FGF13一直高水平表达,其主要有两个剪接体亚型,FGF13A具

【相似文献】