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青蛙骨骼肌细胞膜上的表面电位变化与兴奋-收缩偶联相关。

A surface potential change in the membranes of frog skeletal muscle is associated with excitation-contraction coupling.

作者信息

Jong D S, Stroffekova K, Heiny J A

机构信息

Department of Molecular and Cellular Physiology, University of Cincinnati, College of Medicine, OH 45267-0576, USA.

出版信息

J Physiol. 1997 Mar 15;499 ( Pt 3)(Pt 3):787-808. doi: 10.1113/jphysiol.1997.sp021969.

Abstract
  1. Voltage changes and intramembrane charge movements in the transverse tubule membranes (T-system) of frog fast twitch muscle fibres were compared using the potentiometric dye WW-375 and a Vaseline-gap voltage clamp. As shown previously, the potentiometric dye reports a dynamic surface potential change that occurs on the myoplasmic face of the T-system membranes when the macroscopic potential applied across the surface membrane exceeds the mechanical threshold (about -60 mV). 2. The voltage dependence of the extra surface potential change and charge movement were found to be similar. Both activated with a sigmoid voltage dependence centred around -35 to -40 mV, and saturated at voltages above 0 mV. Both processes inactivated upon sustained depolarization, with a mid-point for inactivation of -40 mV. 3. Pharmacological agents which alter charge movement and excitation-contraction (E-C) coupling altered the non-linear surface potential change in a parallel manner. Perchlorate, which potentiates charge movement and E-C coupling, slowed the activation and deactivation of both charge movement and the non-linear surface potential change at voltages above -40 mV, and shifted the voltage dependence of both processes by 13 14 mV to more negative voltages. Dantrolene, which depresses charge movement and E-C coupling, shifted the voltage dependence of both processes to more positive voltages. Nifedipine, which suppresses charge movement and E-C coupling, reduced the magnitude of both charge movement and the non-linear surface potential change. 4. The non-linear surface potential change remained after the sarcoplasmic reticulum (SR) was depleted of Ca2+, suggesting that it is not a consequence of Ca2+ release. 5. These results suggest that the non-linear surface potential change is closely associated with movements of the voltage sensor (dihydropyridine (DHP) receptor) that control E-C coupling and/or signal transduction across the triadic junction. We propose that the movement of charged intramembrane domains of the DHP receptor which generate charge movement drive a subsequent movement of charged intracellular molecular domains that move within about 1 nm of the T-system membrane to generate a measurable change in surface charge. For example, the postulated mobile surface charges could be on an intracellular domain of the voltage sensor or closely associated protein, or could be a charged molecular domain of a protein that associates/dissociates with T-system membrane or DHP receptor during E-C coupling.
摘要
  1. 使用电位染料WW - 375和凡士林间隙电压钳,比较了青蛙快肌纤维横管膜(T系统)中的电压变化和膜内电荷移动。如先前所示,当施加在表面膜上的宏观电位超过机械阈值(约 - 60 mV)时,电位染料报告了T系统膜肌质面上发生的动态表面电位变化。2. 发现额外表面电位变化和电荷移动的电压依赖性相似。两者均以约 - 35至 - 40 mV为中心呈S形电压依赖性激活,并在高于0 mV的电压下饱和。持续去极化时,这两个过程均失活,失活中点为 - 40 mV。3. 改变电荷移动和兴奋 - 收缩(E - C)偶联的药理剂以平行方式改变非线性表面电位变化。高氯酸盐增强电荷移动和E - C偶联,在高于 - 40 mV的电压下减缓电荷移动和非线性表面电位变化的激活和失活,并使这两个过程的电压依赖性向更负的电压移动13 - 14 mV。丹曲林抑制电荷移动和E - C偶联,使这两个过程的电压依赖性向更正的电压移动。硝苯地平抑制电荷移动和E - C偶联,降低电荷移动和非线性表面电位变化的幅度。4. 肌浆网(SR)中的Ca2 +耗尽后,非线性表面电位变化仍然存在,这表明它不是Ca2 +释放的结果。5. 这些结果表明,非线性表面电位变化与控制E - C偶联和/或跨三联体连接信号转导的电压传感器(二氢吡啶(DHP)受体)的移动密切相关。我们提出产生电荷移动的DHP受体带电膜内结构域的移动驱动了带电细胞内分子结构域的后续移动,这些分子结构域在T系统膜约1 nm范围内移动以产生可测量的表面电荷变化。例如,假定的移动表面电荷可能位于电压传感器或紧密相关蛋白质的细胞内结构域上,或者可能是在E - C偶联期间与T系统膜或DHP受体缔合/解离的蛋白质的带电分子结构域。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f97/1159295/38ecdc2f3577/jphysiol00284-0228-a.jpg

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