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A study on neural plasticity mechanisms of nociceptive transmission induced by peripheral trigeminal nerve injury

周围三叉神经损伤所致伤害性感受传递的神经可塑性机制研究

基本信息

批准号：
14370665
负责人：
SEO Kenji
金额：
$ 7.74万
依托单位：
Niigata University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14370665/
关键词：
trigeminal Caudalis membrane excitation substance p NK1 receptor potential development abnormal sensation nociception trigeminal development substance P caudalis paresthesia Current perception threshold neuropathy sensory imp

项目摘要

1.Optical analysis of membrane potentials in the t trigeminal nociceptive afferent inputs transmission center subnucleus caudalis (Vc) with a high speed recording technique.(1)It was observed that single stimulation to the trigeminal spinal tract produced excitation transmission with short duration in the Vc, which was mediated by AMPA/Kinate type glutamate receptor.(2)It was observed that NK 1 and NMDA receptors were involved in the large and long continuing excitation propagation within the Vc caused by electrical stimulation to the trigeminal spinal tract (Tr).(3)Different developmental changes in the excitation propagation features were observed.(4)Nociceptive stimuli formalin injection to the cheek produced an enlargement of excitation propagation in the Vc by single stimuli to the Tr.2.Immunohistochemical study of the spatial distributions of the substance p and NK1 receptor.(1)Substance P and NK1 receptor were distributed in the superficial layer of the Vc and deep layer in the postnatal week 1.(2)This distribution pattern changed in the postnatal developmental periods, meaning that neuropeptide relating neural excitation mechanism develops postnatally.3.Clinical observations of the abnormal sensation caused by peripheral nerve injury.(1)Spontaneous paresthesia and elicited paresthesia showed different sequential changes after the injury.(2)Current perception threshold measurements can differentiate damage of Aβ,Aδ, and C fiber. This measurement showed that abnormal sensations related to the dysfunction of the Aβ and C fiber and especially C-fiber damage can relate to the establishment of a part of the abnormal sensations, elicited paresthesia.Combined with these results, it was suggested that peripheral nerve injury relates to neuropeptide from the afferent terminals in the Vc and this can contribute to establish and maintain some abnormal sensations for a long period after nerve injury.

1.三叉神经伤害性传入神经传递中心尾侧亚核（Vc）膜电位的高速记录光学分析。(1)It结果表明，单次刺激三叉神经脊束可使Vc产生短时间的兴奋传递，这种兴奋传递是由AMPA/Kinate型谷氨酸受体介导的。(2)It电刺激三叉神经脊束（Tr）引起的Vc内大而长的连续兴奋传播，与NK 1和NMDA受体有关。（3）不同发育阶段的兴奋传播特征发生了不同程度的变化。（4）伤害性刺激后，单次刺激三叉神经，可使Vc兴奋性传播扩大。2.免疫组织化学研究P物质和NK_1受体的空间分布。（1）生后1周，P物质和NK 1受体分布于Vc浅层和深层。（2）这种分布模式在出生后发育阶段发生变化，说明与神经兴奋机制有关的神经肽在出生后发育。3.周围神经损伤引起的感觉异常的临床观察。（1）自发性感觉异常和诱发性感觉异常在伤后表现出不同的时序性变化。（2）电流感觉阈值的测定可以区分Aβ、Aδ和C纤维的损伤。这一测量结果表明，与Aβ和C纤维功能障碍有关的异常感觉，特别是C纤维损伤，可以与部分异常感觉的建立有关，引起感觉异常。提示周围神经损伤与Vc内传入终末的神经肽有关，这可能有助于某些异常感觉的建立和长期维持。神经损伤