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重症肌无力患者胸腺及胸腺瘤上皮细胞中乙酰胆碱诱导电流缺失。

Absence of acetylcholine-induced current in epithelial cells from thymus glands and thymomas of myasthenia gravis patients.

作者信息

Siara J, Rüdel R, Marx A

机构信息

Abteilung für Allgemeine Physiologie, Universität Ulm, FRG.

出版信息

Neurology. 1991 Jan;41(1):128-31. doi: 10.1212/wnl.41.1.128.

Abstract

We investigated the activity of ion channels in epithelial cells from human thymus glands and thymomas kept in short-term cell culture by clamping the membrane potential of the cells at -85 mV and determining the membrane current flowing on application of acetylcholine, glycine, or gamma-aminobutyric acid. In concentrations of up to 10(-3) M, none of the neurotransmitters induced any detectable current. This suggests (1) that there are no acetylcholine receptors (AChRs) or other products of the AChR gene family having ion-channel properties in the membranes of these epithelial cells, and (2) that the alpha-bungarotoxin-binding protein of thymus and thymoma has no AChR-like ion-channel property. These results support the hypothesis that the cross-reacting structures that elicit the anti-AChR autoimmune response in thymoma-associated myasthenia gravis are antigens having only limited homology with the AChR. Myasthenia gravis not associated with thymoma might have a different pathogenesis.

摘要

我们通过将细胞的膜电位钳制在 -85 mV 并测定施加乙酰胆碱、甘氨酸或γ-氨基丁酸时流动的膜电流,研究了短期细胞培养中保存的人胸腺和胸腺瘤上皮细胞中离子通道的活性。在浓度高达 10(-3) M 时,这些神经递质均未诱导出任何可检测到的电流。这表明:(1)这些上皮细胞膜中不存在乙酰胆碱受体(AChRs)或具有离子通道特性的 AChR 基因家族的其他产物;(2)胸腺和胸腺瘤的α-银环蛇毒素结合蛋白不具有类似 AChR 的离子通道特性。这些结果支持以下假设:在胸腺瘤相关的重症肌无力中引发抗 AChR 自身免疫反应的交叉反应结构是与 AChR 仅有有限同源性的抗原。与胸腺瘤无关的重症肌无力可能具有不同的发病机制。

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