Involvement of neurotrophic factors in the development of neuropathic pain evoked by the loose-ligation of peripheral nerves

神经营养因子参与周围神经松动结扎引起的神经性疼痛的发生

基本信息

批准号：
20592183
负责人：
YONEHARA Norifumi
金额：
$ 2.75万
依托单位：
Ohu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2008
资助国家：
日本
起止时间：
2008 至 2010
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20592183/
关键词：
疼痛神経因性疼痛神経栄養因子熱侵害刺激逃避行動求心路遮断性疼痛アロディニア痛覚過敏マイクロダイアリシスグルタミン酸ノルアドレナリン高速クロマトグラフィー電気検出器 von Freyフィラメント高速クロマトグラフィ-電気化学検出器

项目摘要

It has been already known that various neurotrophic factors act on the repair of the damage site for neuronal regeneration following a peripheral nerve injury. In this study, therefore, to investigate whether or not neurotrophic factors affected the development and/or maintenance of such pathological pain states as the hyperalgesia and allodynia observed with peripheral nerve damage, loose-ligation on the left sciatic nerves of mouse were performed. The responses to thermal stimulation were then measured by the Plantar Test. Hypersensitivity to thermal stimulation developed on the ipsilateral side in ligated animals 3 days after surgery and lasted for at least 49 days. The direct application of neurotrophic factors such as oxidized galectin-1, artemin and platelet-derived neurotrophic factor (BDNF) at the nerve-ligation site showed remarkable inhibition against nerve injury-induced thermal hyperalgesia compared with the direct application of vehicle. Particularly, in the oxidized galectin-1 application group, marked analgesic effect was observed 3-28 days after application of this drug, that is, thermal hyperalgesia developed on the 31 days after injury. Unlike such result obtained by the oxidized galectin-1, however, in the group which applied artemin or platelet-derived neurotrophic factor (BDNF), prolongation of withdrawal latency (analgesic effect) was not observed

众所周知，各种神经营养因子作用于周围神经损伤后神经元再生的损伤部位的修复。因此，在这项研究中，为了研究神经营养因素是否影响是否影响和/或维持病理疼痛状态，例如在外周神经损伤中观察到的痛性和异常性疼痛，对小鼠的左坐骨神经进行了松散结合。然后通过足底测试测量对热刺激的反应。手术后3天，在结扎动物的同侧产生了对热刺激的高敏性，并且至少持续了49天。在神经结扎部位，神经营养因子的直接应用，例如氧化的lectectin-1，Artemin和血小板衍生的神经营养因子（BDNF），表现出明显的抑制作用，对神经损伤诱导的热过敏症与直接应用相比。特别是，在氧化的Galectin-1施用组中，在施用该药物后3-28天观察到明显的镇痛作用，即在损伤后31天发育的热痛觉过敏。但是，与氧化的lectectin-1获得的结果不同，在应用artemin或血小板衍生的神经营养因子（BDNF）的组中，未观察到戒断潜伏期的延长（镇痛作用）