Calderón Juan C, Bolaños Pura, Caputo Carlo
Physiology and Biochemistry Research Group-Physis, Department of Physiology and Biochemistry, Faculty of Medicine, University of Antioquia UdeA, Calle 70 No 52-21, Medellín, Colombia.
Laboratory of Cellular Physiology, Centre of Biophysics and Biochemistry, Venezuelan Institute for Scientific Research (IVIC), Caracas, Venezuela.
Biophys Rev. 2014 Mar;6(1):133-160. doi: 10.1007/s12551-013-0135-x. Epub 2014 Jan 24.
First coined by Alexander Sandow in 1952, the term excitation-contraction coupling (ECC) describes the rapid communication between electrical events occurring in the plasma membrane of skeletal muscle fibres and Ca release from the SR, which leads to contraction. The sequence of events in twitch skeletal muscle involves: (1) initiation and propagation of an action potential along the plasma membrane, (2) spread of the potential throughout the transverse tubule system (T-tubule system), (3) dihydropyridine receptors (DHPR)-mediated detection of changes in membrane potential, (4) allosteric interaction between DHPR and sarcoplasmic reticulum (SR) ryanodine receptors (RyR), (5) release of Ca from the SR and transient increase of Ca concentration in the myoplasm, (6) activation of the myoplasmic Ca buffering system and the contractile apparatus, followed by (7) Ca disappearance from the myoplasm mediated mainly by its reuptake by the SR through the SR Ca adenosine triphosphatase (SERCA), and under several conditions movement to the mitochondria and extrusion by the Na/Ca exchanger (NCX). In this text, we review the basics of ECC in skeletal muscle and the techniques used to study it. Moreover, we highlight some recent advances and point out gaps in knowledge on particular issues related to ECC such as (1) DHPR-RyR molecular interaction, (2) differences regarding fibre types, (3) its alteration during muscle fatigue, (4) the role of mitochondria and store-operated Ca entry in the general ECC sequence, (5) contractile potentiators, and (6) Ca sparks.
“兴奋-收缩偶联”(ECC)一词由亚历山大·桑多在1952年首次提出,它描述了骨骼肌纤维质膜中发生的电活动与肌浆网释放钙之间的快速通讯,这种通讯会导致肌肉收缩。骨骼肌单收缩过程中的一系列事件包括:(1)动作电位沿质膜的起始和传播;(2)电位在整个横管系统(T管系统)中的扩散;(3)二氢吡啶受体(DHPR)介导的膜电位变化检测;(4)DHPR与肌浆网(SR)兰尼碱受体(RyR)之间的变构相互作用;(5)钙从SR释放以及肌浆中钙浓度的瞬时增加;(6)肌浆钙缓冲系统和收缩装置的激活,随后是(7)肌浆中钙的消失,这主要是通过SR钙腺苷三磷酸酶(SERCA)将其重新摄取到SR中实现的,并且在某些情况下会转运到线粒体并由钠钙交换体(NCX)排出。在本文中,我们回顾了骨骼肌兴奋-收缩偶联的基础知识以及用于研究它的技术。此外,我们强调了一些最新进展,并指出了与兴奋-收缩偶联相关的特定问题上的知识空白,例如(1)DHPR-RyR分子相互作用;(2)纤维类型的差异;(3)肌肉疲劳期间的变化;(4)线粒体和储存-操作性钙内流在一般兴奋-收缩偶联序列中的作用;(5)收缩增强剂;以及(6)钙火花。