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银离子诱导青蛙骨骼肌纤维的张力发展和膜去极化。

Silver ion-induced tension development and membrane depolarization in frog skeletal muscle fibres.

作者信息

Oba T, Hotta K

出版信息

Pflugers Arch. 1985 Dec;405(4):354-9. doi: 10.1007/BF00595688.

DOI:10.1007/BF00595688
PMID:3878495
Abstract

Silver ions elicit dose-dependently a transient contracture in single fibres of bull-frog toe muscle placed in 0-Ca2+, Cl- -free MOPS solution containing 3 mM Mg2+ and NO3-. To elucidate the mechanisms involved, changes in membrane potential and in tension development were continuously measured following exposure to Ag+. The effect of Ag+ on contraction in fibres in which the membrane had been depolarized by elevating the external K+ concentration was also examined. The major findings of this investigation are as follows. (1) The mechanical threshold was shifted towards more negative potentials by 5 mV (-51 to -56 mV), when Ca2+ and Cl- in the Ringer's solution were replaced with Mg2+ and NO3-, respectively. (2) On the exposure of the fibres to 5 microM Ag+, the membrane potential decreased by 1.6 mV from -87.8 mV and tension was developed. (3) In fibres soaked in a solution containing 10 mM K+ (corresponding to a membrane potential of -69.5 mV), 5 microM Ag+ produced a large contracture similar to that seen in the control solution. (4) The Ag+-induced contracture was inactivated when more than 20 mM K+ was used. (5) The membrane depolarization evoked by either 20 or 50 microM Hg2+ did not produce contraction. (6) Muscle fibres which had been exposed to 20 microM Hg2+ for 5 min responded to 5 microM Ag+ by a transient tension development. These findings strongly suggest that Ag+-induced tension development is not associated with depolarization of the surface membrane but rather is caused by specific actions of Ag+ on membrane proteins in the T-tubules.

摘要

银离子在置于含3 mM镁离子和硝酸根离子的0钙离子、无氯离子的MOPS溶液中的牛蛙趾肌单纤维中,剂量依赖性地引发短暂收缩。为阐明其中涉及的机制,在暴露于银离子后,连续测量膜电位和张力发展的变化。还研究了银离子对通过提高外部钾离子浓度使膜去极化的纤维收缩的影响。本研究的主要发现如下:(1)当林格氏溶液中的钙离子和氯离子分别被镁离子和硝酸根离子取代时,机械阈值向更负的电位移动了5 mV(从-51 mV到-56 mV)。(2)当纤维暴露于5 microM银离子时,膜电位从-87.8 mV下降了1.6 mV,并产生了张力。(3)在浸泡于含10 mM钾离子溶液(对应膜电位为-69.5 mV)的纤维中,5 microM银离子产生了与对照溶液中相似的大收缩。(4)当使用超过20 mM钾离子时,银离子诱导的收缩被灭活。(5)20或50 microM汞离子引起的膜去极化未产生收缩。(6)暴露于20 microM汞离子5分钟的肌肉纤维对5 microM银离子产生短暂的张力发展反应。这些发现强烈表明,银离子诱导的张力发展与表面膜的去极化无关,而是由银离子对横管中膜蛋白的特异性作用引起的。

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本文引用的文献

1
SARCOPLASMIC RETICULUM. I. THE UPTAKE OF CA++ BY SARCOPLASMIC RETICULUM FRAGMENTS.肌浆网。一、肌浆网片段对钙离子的摄取。
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Potassium contractures in single muscle fibres.单根肌纤维中的钾挛缩
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External calcium and contractile activation during potassium contractures in twitch muscle fibres of the frog.青蛙单收缩肌纤维钾挛缩期间的细胞外钙与收缩激活
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Effect of Ag+ on membrane permeability of perfused Helix pomatia neurons.银离子对灌注的苹果螺神经元膜通透性的影响。
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7
Modulation of the Ca2+ channel voltage sensor and excitation-contraction coupling by silver.银对钙离子通道电压传感器及兴奋-收缩偶联的调节作用
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8
Sulphydryl reagents trigger Ca2+ release from the sarcoplasmic reticulum of skinned rabbit psoas fibres.巯基试剂可触发去表皮兔腰大肌纤维肌浆网释放钙离子。
J Physiol. 1992 Aug;454:389-420. doi: 10.1113/jphysiol.1992.sp019270.
Can J Physiol Pharmacol. 1982 Apr;60(4):513-23. doi: 10.1139/y82-071.
4
Induced Ca2+ release in skeletal muscle sarcoplasmic reticulum by sulfhydryl reagents and chlorpromazine.巯基试剂和氯丙嗪诱导骨骼肌肌浆网中钙离子释放
Arch Biochem Biophys. 1983 Mar;221(2):458-66. doi: 10.1016/0003-9861(83)90164-9.
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Mechanical, electrical, and morphological characteristics of skeletal muscle fibers from Xenopus and other species of frogs.
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