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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Modulation of sensory neuron mechanotransduction by PKC- and nerve growth factor-dependent pathways
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Modulation of sensory neuron mechanotransduction by PKC- and nerve growth factor-dependent pathways

机译：PKC和神经生长因子依赖性途径对感觉神经元机械传导的调节

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摘要

Many sensations of pain are evoked by mechanical stimuli, and in inflammatory conditions, sensitivity to such stimuli is commonly increased. Here we used cultured sensory neurons as a model of the peripheral terminal to investigate the effects of inflammatory signaling pathways on mechanosensitive ion channels. Activation of two of these pathways enhanced transduction in a major population of nociceptors. The proinflammatory neurotrophin nerve growth factor caused an up-regulation of mechanically activated currents via a transcriptional mechanism. Activators of PKC, given in vitro and in vivo, also caused an increase in mechanically activated membrane current and behavioral sensitization to mechanical stimulation, respectively. The effect of activating PKC was inhibited by tetanus toxin, suggesting that insertion of new channels into the cell membrane is involved in sensitization. These results reveal previously undescribed mechanisms by which PKC and nerve growth factor synergistically enhance the response of nociceptors to mechanical stimuli, suggesting possible targets for pain treatment.
机译：机械刺激引起许多疼痛感，并且在炎症条件下，通常会增加对这种刺激的敏感性。在这里，我们使用培养的感觉神经元作为周围末端的模型，以研究炎症信号通路对机械敏感离子通道的影响。这些途径中的两种途径的激活增强了主要伤害感受器的转导。促炎性神经营养蛋白神经生长因子通过转录机制引起机械激活电流的上调。体外和体内给予的PKC激活剂也分别导致机械激活的膜电流和对机械刺激的行为敏感性增加。破伤风毒素可抑制激活PKC的作用，这表明新通道插入细胞膜与致敏有关。这些结果揭示了PKC和神经生长因子协同增强伤害感受器对机械刺激的反应的先前未曾描述的机制，为疼痛治疗提供了可能的靶标。

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