Study on the peripheral mechanism of noiceptor sensitization using excitability test
Study on the peripheral mechanism of noiceptor sensitization using excitability test
批准号:
08680886
负责人:
MIZUMURA Kazue
金额:
$1.41万
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
项目状态:
已结题
起止时间:
1996 至 1997
中文摘要
为了评价终末去极化是否在炎症介质致敏伤害感受器中起重要作用,在感受部位进行了兴奋性试验。单纤维活动记录在体外使用犬睾丸精索神经制剂。在机械敏感区绘制电兴奋性图,并在兴奋阈值最低的部位进行兴奋性测试。高K^+溶液(12.18 mM)通常被认为会引起去极化,它会引起短暂的放电,同时伴随着兴奋阈值的降低(兴奋性的增加),但在这种变化中没有观察到明显的浓度依赖性。缓激肽(3 nM)既不引起放电,也不改变兴奋阈值。当缓激肽10 nM或更高时,其仅诱导放电的少量增加,而当其诱导放电的明显增加时,其诱导兴奋阈值的增加。这些结果表明,放电的碰撞起源于兴奋性试验的部位和其他接受部位。为了避免这种情况,已经开发了电极内灌注系统,并且对暴露于输注溶液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10 μ M的兴奋降低。用这种方法,缓激肽只引起短暂的放电是典型的。低浓度缓激肽的作用有待研究。这种内电极灌注方法提供了一种新的方法,用荧光染料可视化的感受性终末纤维。
英文摘要
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.
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Mizumura, K.: "Peripheral mechanism of hyperalgesia-Sensitization of nociceptors." Nagoya Journal of Medical Sciences. 60. 69-87 (1997)
Mizumura, K.:“痛觉过敏的外周机制——伤害感受器的敏化。”
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通讯作者:
Mizumura, K.: "Natural history of nociceptor sensitization -The search for a peripheral mechanism of hyperalgesia-." Pain Review(in press). (1998)
Mizumura, K.:“伤害感受器敏化的自然史 - 寻找痛觉过敏的外周机制 -”。
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Mizumura, K., et al.: "Opposite effects of increased intracellular cyclic AMP in the heat and bradykinin responses of canine visceral polymodal receptors in vitro." Neuroscience Research. 25. 335-341 (1996)
Mizumura, K. 等人:“细胞内环 AMP 增加对犬内脏多模式受体体外热和缓激肽反应的相反影响。”
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Mizumura,K., et al.: "Conditions for vitally staining the nerve terminals of the various tissues in various species." Environmental Medicine. 40. 149-152 (1996)
Mizumura,K. 等人:“对不同物种的不同组织的神经末梢进行活体染色的条件。”
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Mizumura, K., et al.: "Modification of nociceptor responses by inflammatory mediators and second messengers implicated in their action - a study in canine testicular polymodal receptors.In:The Polymodal Receptor - A Gateway to Pathological Pain" Amsterdam
Mizumura, K. 等人:“炎症介质和与其作用相关的第二信使对伤害性感受器反应的改变 - 一项针对犬睾丸多模式受体的研究。In:多模式受体 - 通往病理性疼痛的门户” 阿姆斯特丹
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海外基金