Nav1.7 sodium channel expression in human lingual nerve neuromas
Nav1.7 sodium channel expression in human lingual nerve neuromas
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DOI：
10.1016/j.archoralbio.2006.11.011
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发表时间：
2007-05-01
影响因子：
3
通讯作者：
Boissonade, F. M.
中科院分区：
文献类型：
--
作者：
Bird, E. V.;Robinson, P. P.;Boissonade, F. M.
目的：在拔除下第三磨牙的过程中，三叉神经的外周分支经常受损，并且一小部分遭受损伤的患者会出现持续的慢性疼痛。疼痛的原因尚不清楚，也没有令人满意的治疗方法。本研究的目的是检查钠通道亚型Na（v）1.7在受损的人舌神经的表达，并确定Na（v）1.7的表达和报告的症状dysaesthesis.Methods：11个神经瘤连续性（NEM）和11个神经端神经瘤（NENs）进行了研究，并获得在手术修复受损的舌神经的时间。根据疼痛、刺痛或不适的程度，将样本分类为从有症状或无症状的患者中获得。结果：Na（v）1.7通道在舌神经瘤中表达。Na（v）1.7的表达水平与患者的感觉障碍症状之间没有直接关系。然而，在小脑扁桃体中，发现Nav1.7和巨噬细胞表达之间呈负相关，在有症状的小脑扁桃体中，发现Na（v）1.7表达和轴突apposition.Conclusions之间存在直接相关性：这些数据表明，Na（v）1.7表达单独在启动疼痛症状的感觉迟钝中不起主要作用。神经病理性疼痛的发展可能涉及复杂的相互作用，包括超微结构和离子通道密度的变化。(c)2006爱思唯尔有限公司保留所有权利。
Objective: Peripheral branches of the trigeminal nerve are often damaged during the removal of lower third molar teeth, and a small proportion of patients who sustain an injury develop persistent chronic pain. The cause of the pain is not clear and there are no satisfactory methods of treatment. The aim of the present study was to examine the expression of the sodium channel subtype Na(v)1.7 in damaged human lingual nerves, and to identify any association between Na(v)1.7 expression and reported symptoms of dysaesthesia.Methods: Eleven neuromas-in-continuity (NICs) and 11 nerve-end neuromas (NENs) were studied, and were all obtained at the time of surgical repair of the damaged lingual nerve. Specimens were categorised as being obtained from patients with symptoms or without symptoms, according to the degree of pain, tingling or discomfort that had been experienced. The tissue was prepared and processed for indirect immunofluorescence, and image analysis was used to quantify the percentage area of PGP 9.5-labelled tissue that also contained Na(v)1.7.Results: The results demonstrated that sodium channel Nav1.7 was expressed in human lingual nerve neuromas. There was no direct relationship between the level of expression of Na(v)1.7 and the patients' symptoms of dysaesthesia. However, in NICs there was found to be an inverse correlation between Nav1.7 and macrophage expression, and in symptomatic NICs a direct correlation was found between Na(v)1.7 expression and axonal apposition.Conclusions: These data suggest that Na(v)1.7 expression alone does not play a primary role in initiating the painful symptoms of dysaesthesia. The development of neuropathic pain may involve complex interactions including changes in ultrastructure and ion channel density. (c) 2006 Elsevier Ltd. All rights reserved.