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骨骼肌离子转运系统与神经支配的关系及其在强直性肌病中的作用。

Ionic transporting systems of skeletal muscle in relation with innervation and their involvement in myotonic diseases.

作者信息

Renaud J F

机构信息

IRIS et Compagnie-Développement, Courbevoie, France.

出版信息

Neurochem Res. 1991 Jun;16(6):669-73. doi: 10.1007/BF00965553.

Abstract

Excitation-contraction coupling describes the series of events that begins with propagated action potential on the muscle fiber surface membrane and leads to the twitch contraction of the fiber. The generation of an action potential during excitation requires rapid sequential changes in membrane conductances of Na+, Ca2+, and K+ ions that depend upon the opening and closing of the respective channels. Myotonic disorders are inherited diseases whose clinical manifestations include electrophysiological signs such as increased excitability and delayed relaxation of the muscles after voluntary contraction. All these disorders appears to be due to an abnormality of the muscle itself since they persist after section or blocking of the motor nerve after curarization. Most experimental and clinical data suggest that human myotonia arises from genetically-induced structural and functional alterations of the muscle membrane. The purpose of this article is to focus on the more recent developments in the molecular and pharmacological analysis of cation transporting systems such as ionic channels and (Na+, K+) ATPase in myotonic disorders.

摘要

兴奋-收缩偶联描述了一系列事件,这些事件始于肌纤维表面膜上传播的动作电位,并导致纤维的抽搐收缩。兴奋过程中动作电位的产生需要Na+、Ca2+和K+离子膜电导的快速顺序变化,这取决于各自通道的开放和关闭。强直性肌营养不良症是遗传性疾病,其临床表现包括电生理体征,如自愿收缩后肌肉兴奋性增加和松弛延迟。所有这些疾病似乎都归因于肌肉本身的异常,因为在箭毒化后切断或阻断运动神经后它们仍然存在。大多数实验和临床数据表明,人类肌强直源于基因诱导的肌膜结构和功能改变。本文的目的是关注强直性肌营养不良症中阳离子转运系统(如离子通道和(Na+,K+)ATP酶)的分子和药理学分析的最新进展。

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