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青蛙缝匠肌的肌管性异常整流

Sarcotubular anomalous rectification of frog sartorius muscle.

作者信息

Takeda K

出版信息

Jpn J Physiol. 1975;25(4):495-506. doi: 10.2170/jjphysiol.25.495.

Abstract

The membrane site responsible for anomalous rectification was determined in frog sartorius muscle fibers. The total current-voltage relation of glycerol-treated fibers which represents mainly the properties of the sarcolemma was linear for membrane potentials between about -90 and -50 mV. Thus moderate depolarization-induced anomalous rectification in intact fibers represents a property of the sarcotubular system. The absence of slow hyperpolarization in glycerol-treated fibers was caused by the abolition of early conductance increase, and the sarcotubular system is responsible for the inward rectifier. Picrotoxin selectively inhibited both moderate depolarization-induced anomalous rectification and hyperpolarization-induced early conductance increase. This suggests that the same component in the sarcotubular system is responsible for these conductance changes. The inhibition with picrotoxin of moderate depolarization-induced anomalous rectification suggests the possibility that it is caused by an electrogenic effect rather than a decrease in K conductance. A sarcolemmal hyperpolarization-activated slow conductance increase was revealed.

摘要

在青蛙缝匠肌纤维中确定了负责反常整流的膜位点。甘油处理过的纤维的总电流-电压关系在膜电位约-90至-50 mV之间呈线性,主要代表肌膜的特性。因此,完整纤维中适度去极化诱导的反常整流是肌管系统的一种特性。甘油处理过的纤维中不存在缓慢超极化是由于早期电导增加的消除,且肌管系统负责内向整流。印防己毒素选择性地抑制了适度去极化诱导的反常整流和超极化诱导的早期电导增加。这表明肌管系统中的同一成分负责这些电导变化。印防己毒素对适度去极化诱导的反常整流的抑制表明,它可能是由电生效应而非钾电导降低引起的。揭示了肌膜超极化激活的缓慢电导增加。

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