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Study on the role of the primary afferent fibers in thedevelopment/maintenance of the intractable pain in the oro-facial region

初级传入纤维在口面部顽固性疼痛发生/维持中的作用研究

基本信息

批准号：
18592030
负责人：
YONEHARA Norifumi
金额：
$ 2.46万
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：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

项目摘要

It is well known that the pathological pain states such as allodynia, hyperalgesia, and phantom pain can result after nerve injury or chronic inflammation. It is also recognized that an increase in the afferent impulse flow from damaged nerve areas enhances the activity of spinal dorsal horn neurons and produces pain. The activation of N-methyl-D-aspartate (NMDA) receptors in spinal dorsal horn neurons is widely regarded to be critical for the development and maintenance of the hyperalgesia induced by nerve injury.Increasing evidence suggests that, at the site of the first synaptic relay of nociceptive pathway, activation of N-methyl-D-aspartate (NMDA) receptors modulates nociceptive transmission via a nitric oxide (NO) pathway. Therefore, to further clarify the central mechanisms underlying the peripheral nerve injury-induced pathological pain in the trigeminal system, this project examined influence of NO to the change in excitatory amino acids (EAAs) level in the superficial layer of subnucleus caudalis of the brain-stem trigeminal sensory nuclear complex (SpVc-I, II) following a ligation injury to the inferior alveolar nerves.A very high EAAs release responses was observed immediately after the start of the perfusion in ligated animals compared with sham-operated rats. The EAA level evoked by application of the 40-V tooth pulp-stimulation or 1% capsaicin cream was significantly higher in the ligated animals than those in the sham-operated animals. This increase of EAAs level induced by capsaicin cream was inhibited by adding carboxy-PTIO, an NO scavenger, to the perfusate.These results suggest that alterations in the stimulus-evoked raised EAA levels that occur in the site of the first synaptic relay of the dental pain pathway and which are expressed via endogenous NO, and which play an important role in development and/or maintenance of pathological pain states following dental peripheral nerve injury

众所周知，病理性疼痛状态如异常性疼痛、痛觉过敏和幻痛可在神经损伤或慢性炎症后产生。还认识到，来自受损神经区域的传入冲动流的增加增强了脊髓背角神经元的活动并产生疼痛。脊髓背角神经元N-甲基-D-天冬氨酸（NMDA）受体的激活被广泛认为是神经损伤后痛敏发生和维持的关键，越来越多的证据表明，在伤害性感受通路的第一突触传递部位，NMDA受体的激活通过一氧化氮（NO）通路调节伤害性感受的传递。因此，为了进一步阐明周围神经损伤后三叉神经系统病理性痛的中枢机制，本研究观察了NO对脑干三叉神经感觉核复合体尾侧亚核浅层兴奋性氨基酸（EAAs）含量的影响与假手术组相比，结扎组大鼠在灌流开始后立即出现极高的EAA释放反应。结扎组动物经40 V牙髓刺激或1%辣椒素乳膏刺激后EAA水平明显高于假手术组。辣椒素乳膏诱导的EAA水平的增加可通过向灌流液中添加一种NO清除剂羧基-PTIO来抑制。这些结果表明，刺激诱发的EAA水平的改变升高发生在牙痛通路的第一个突触中继部位，并通过内源性NO表达，并且在牙齿周围神经损伤后病理性疼痛状态的发展和/或维持中起重要作用