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补骨脂素、苯并呋喃、吖啶酮和香豆素对完整有髓神经纤维离子电流的作用方式及其在脱髓鞘疾病中的意义。

Mode of action of psoralens, benzofurans, acridinons, and coumarins on the ionic currents in intact myelinated nerve fibres and its significance in demyelinating diseases.

作者信息

Bohuslavizki K H, Hänsel W, Kneip A, Koppenhöfer E, Niemöller E, Sanmann K

机构信息

Institute of Physiology, University of Kiel, Germany.

出版信息

Gen Physiol Biophys. 1994 Aug;13(4):309-28.

PMID:7890147
Abstract

The actions of psoralens, benzofurans, acridinons and coumarins on the ionic currents in intact myelinated nerve fibres were investigated. All 6 substances blocked the potassium currents in a time-dependent manner, producing so-called K+ transients. Only 5-methoxypsoralen is a largely selective blocker of predominantly the axolemmal potassium channels, which is the characteristic required by our previously proposed working hypothesis for the mechanism of potassium-channel blockers in demyelinating diseases, in particular multiple sclerosis. If the observed K+ transients were to arise by blocking of the potassium channels of the Schwann cell, that is, by the periaxonal accumulation of K+ and a resulting collapse of the electromotive driving force for potassium-ions, according to a modified version of our previous hypothesis the other substances tested could also have a beneficial effect on the impaired impulse conduction in demyelinated axons. In this case a large number of new potential drugs would be available for the symptomatic therapy of MS.

摘要

研究了补骨脂素、苯并呋喃、吖啶酮和香豆素对完整有髓神经纤维离子电流的作用。所有6种物质均以时间依赖性方式阻断钾电流,产生所谓的K +瞬变。只有5-甲氧基补骨脂素主要是轴膜钾通道的选择性阻滞剂,这是我们先前提出的脱髓鞘疾病,特别是多发性硬化症中钾通道阻滞剂机制的工作假设所要求的特征。如果观察到的K +瞬变是通过阻断施万细胞的钾通道而产生的,即通过轴周K +的积累以及由此导致的钾离子电动势驱动力的崩溃,根据我们先前假设的修改版本,其他测试物质也可能对脱髓鞘轴突中受损的冲动传导产生有益影响。在这种情况下,将有大量新的潜在药物可用于MS的对症治疗。

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Mode of action of psoralens, benzofurans, acridinons, and coumarins on the ionic currents in intact myelinated nerve fibres and its significance in demyelinating diseases.补骨脂素、苯并呋喃、吖啶酮和香豆素对完整有髓神经纤维离子电流的作用方式及其在脱髓鞘疾病中的意义。
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