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hNa_v1.8通道蛋白在三叉神经痛痛支神经超微结构中的表达及意义

Expression of hNa_v1.8 channel protein in affected nerve ultrastructure of patients with trigeminal neuralgia
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摘要 目的:观察三叉神经痛(trigeminal neuralgia, TN)患者痛支神经的有髓纤维脱髓鞘处是否有河豚毒素不敏感型(tetrodo toxin resistant, TTX R)hNav1.8通道蛋白的异常表达,探讨其与三叉神经痛的关系。方法:以6例原发性TN第三支痛经保守治疗无效行手术治疗患者的下牙槽神经为研究对象,以舌颌颈联合根治术患者的耳大神经、下牙槽神经为阴性和正常对照,以鼠脊神经为阳性对照,运用免疫组化的方法观察hNav1.8通道蛋白在TN患者痛支神经与对照神经标本超微结构中的表达。结果:hNav1.8通道蛋白在TN患者痛支神经的有髓纤维脱髓鞘处有大量表达,鼠脊神经轴突内有少量表达,而正常下牙槽神经及耳大神经中无表达。结论:hNav1.8通道蛋白在TN患者痛支有髓纤维脱髓鞘处的异常表达可能与TN的发病有关。 Objective:To observe whether there is abnormal expression of tetrodotoxin-resistant (TTX-R)hNa v1.8 channel protein in demyelinated fibers of the affected nerves in patients with trigeminal neuralgia(TN), and to explore the relationship between ectopic discharges and TN.Methods: Six affected inferior alveolar nerves obtained from patients with idiopathic TN were studied. One great auricular nerve and one normal inferior alveolar nerve were used,which were obtained from patients undergoing combined radical neck dissection with glossectomy (negative control) and mandibulectomy (normal controls) . One rat spinal nerve was used as positive control. Immunohistochemical method and electron microscope were used to observe the expression of TTX-R hNa v1.8 channel protein in all groups. Results: Strong expression of hNa v1.8 channel protein was found in the demyelinated fibers of the affected nerves in patients with TN, weak expression in the neuraxon of rat spinal nerve,and none in the normal inferior alveolar nerve and the great auricular nerve. Conclusion: Abnormal expression of hNa v1.8 channel protein in the demyelinated fibers in patients with TN may play an important role in the pathogenesis of TN.
出处 《第二军医大学学报》 CAS CSCD 北大核心 2005年第4期429-431,共3页 Academic Journal of Second Military Medical University
基金 全军医药卫生科研"九五"规划课题(98M084).
关键词 hNav1.8通道蛋白 三叉神经痛 超微结构 免疫组织化学 sodium channel protein 1.8 trigeminal neuralgia ultrastructure immunohistochemistry
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