权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Study on the peripheral mechanism of noiceptor sensitization using excitability test

兴奋性试验研究伤害感受器敏化的外周机制

基本信息

批准号：
08680886
负责人：
MIZUMURA Kazue
金额：
$ 1.41万
依托单位：
Nagoya University, Research Institute of Environmental Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

项目摘要

To evaluate whether terminal depolarization plays an important role in nociceptor sensitization by inflammatory mediators, excitability test at the receptive cite was carried out. Single fiber activities were recorded in vitro using canine testis-spermatic nerve preparations. Electrical excitability was mapped in the mechanically sensitive area, and excitability test was carried out at the spot where the excitation threshold was the lowest. High K^+ solutions (12,18 mM), which is commonly known to induce depolarization, induced brief discharges with concomitant decrease in excitation threshold (increase in excitability), but no clear dependency on the concentration was observed in this change. Bradykinin (3nM) induced neither discharges nor change in excitation threshold. Bradykinin 10nM or higher induced a decrease in excitation threshold when it induced only small increase in discharges while it induced an increase in excitation threshold when it induced a clear increase in descharges. These results suggest a posaibility that collision of discharges originated from the site where excitability test was carried out and from other receptive cites. To avoid this an intra-electrode perfusion system has been developed, and chemical stimulation to limited area which is exposed to infusion solution was carried out. With this method as well, no decrease in excitation by bradykinin 10muM was observed. It was typical that only short-lasting discharges were induced by bradykinin with this method. Effects of bradykinin at lower concentrations were left open to study. This intra-electrode perfusion method provided a new method for visualizing the receptive terminal fibers with a fluorescent dye.

为探讨末端去极化是否在炎性介质对伤害性感受器的敏化中起重要作用，我们在感受端进行了兴奋性测试。用犬睾丸-精索神经标本记录单个纤维的活动。在机械敏感区绘制电兴奋性图，并在兴奋阈值最低处进行兴奋性测试。高K~(++)溶液(12，18 mM)引起短暂放电，伴随着激发阈值的降低(兴奋性增加)，但这种变化没有明显的浓度依赖性。缓激肽(3 Nm)既不引起放电，也不改变兴奋阈值。10 nm或更高的缓激肽仅引起少量放电增加时，激发阈值降低，而引起放电明显增加时，激发阈值增加。这些结果表明，放电的碰撞可能来自进行兴奋性测试的部位和其他接受性CITE。为了避免这种情况，已经开发了电极内灌流系统，并对暴露在输液中的有限区域进行化学刺激。用这种方法，也没有观察到缓激肽10µM对兴奋性的影响。采用这种方法，典型的是缓激肽只能诱发短暂的放电。较低浓度的缓激肽的作用有待研究。这种电极内灌流方法为用荧光染料显示感受性终末纤维提供了一种新的方法。