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秋水仙碱可阻止慢性脱髓鞘时神经传导的恢复。

Colchicine prevents recovery of nerve conduction at chronic demyelination.

作者信息

Liverant S, Meiri H

机构信息

Department of Physiology and Biophysics, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.

出版信息

Brain Res. 1990 Jun 11;519(1-2):50-6. doi: 10.1016/0006-8993(90)90059-k.

Abstract

A colchicine cuff was applied to rat sciatic nerve proximal to a demyelinating region produced by a focal injection of lysophosphatidylcholine (LPC). The colchicine cuff prevented the recovery of function normally seen within 6-8 days after LPC-induced demyelination. Colchicine blocked the delivery of sodium channels to the demyelinated region and induced their accumulation proximal to the cuff. The dual effect of colchicine in blocking both the recovery of impulse propagation through the demyelinated region and the delivery of sodium channels suggests a central role for fast axonal transport of sodium channels in the recovery of function at demyelination.

摘要

将秋水仙碱套环应用于大鼠坐骨神经,该神经靠近通过局部注射溶血磷脂酰胆碱(LPC)产生的脱髓鞘区域。秋水仙碱套环阻止了在LPC诱导脱髓鞘后6 - 8天内通常可见的功能恢复。秋水仙碱阻断了钠通道向脱髓鞘区域的运输,并诱导它们在套环近端积累。秋水仙碱在阻断通过脱髓鞘区域的冲动传导恢复和钠通道运输方面的双重作用表明,钠通道的快速轴突运输在脱髓鞘功能恢复中起核心作用。

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