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What is the mechanism for paresthesia following nerve injury?

神经损伤后感觉异常的机制是什么？

基本信息

批准号：
17592068
负责人：
SEO Kenji
金额：
$ 2.24万
依托单位：
Niigata University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17592068/
关键词：
nerve injury trigeminal paresthesia peptide substance p optical imaging capsaicin mice peptide optical imaging mechanical touch threshold unmyelinated fiber caudalis

项目摘要

1.Immuno-histochemical study : Temporo-spatial changes of substance P distribution in the trigeminal caudalis after nerve injury(1)Neonatal capsaicin treatment induces a disappearance of substance p in deep part of the trigeminal caudalis (Vc) in adult and a transient decrease of substance p in superficial layers of the Vc recovered at 2 weeks of age.(2)This emerged substance p in superficial layers of the Vc does not have any immunoreactivity either for N-200 (the marker for myelinated fiber) or IB4 (the marker for non-peptidergic neuron).These results suggest that neonatal capsaicin treatment induces a long term deficit in nociceptive transmission in the Vc and it is caused by unavailability of neurotransmitter releasing but not by an disappearance of neural transmitters.2.Behavioral study : Long term observation of changes in the mechanical-touch threshold after partial injury of mental nerve(1)Ligation of the mental nerve in mice induces an apparent elevation of mechanical touch threshold just after nerve injury and this state lasts for 1 week.(2)This elevation of the threshold decreases around 1 weeks and relative high level of the threshold remains for 4 weeks. After that, this elevation decreases and reaches to the control level.(3)Changes in the threshold of this animal model look similar to clinical observation of peripheral nerve injury.Combined with these results, it was suggested that peripheral nerve injury relates to neuropeptide from the afferent terminals in the Vc and mechanism for sensory impairment following nerve injury and its recovery has some relationships to change in the neuropeptide.

1.免疫组化研究：神经损伤后三叉神经尾侧核内P物质分布的时空变化（1）新生儿辣椒素处理后，成年三叉神经尾侧核深层P物质消失，而三叉神经尾侧核浅层P物质含量短暂减少，2周龄时恢复。（2）Vc浅层出现的P物质对N-200也无免疫反应性（有髓纤维的标志物）或IB 4（非肽能神经元的标志物）这些结果表明，新生儿辣椒素治疗诱导Vc中伤害性传递的长期缺陷，这是由神经递质释放的不可用性引起的，而不是由神经递质的消失引起的。2.行为学研究：部分损伤颏神经后机械触觉阈值变化的长期观察（1）小鼠颏神经结扎后，机械触觉阈值在神经损伤后即刻明显升高，并持续1周。（2）1周左右阈值的升高逐渐降低，并在4周内保持较高的阈值。之后，该高程降低并达到控制水平。（3）该动物模型的阈值变化与临床观察的周围神经损伤相似，提示周围神经损伤与Vc内传入终末的神经肽有关，神经损伤后感觉障碍及其恢复的机制与Vc内神经肽的变化有一定关系。