Abstract：
The expression excitation-contraction (EC) coupling in skeletal muscle was coined in 1952 (1). The term evolved narrowly to include only the processes at the triad that intervene between depolarization of the transverse tubular (T-tubular) membrane and Ca2+ release from the sarcoplasmic reticulum (SR). From 1970 to 1988, the foundation of EC coupling was elucidated. The channel through which Ca2+ was released during activation was located in the SR by its specific binding to the plant insecticide ryanodine. This channel was called the ryanodine receptor (RyR). The RyR contained four subunits that together constituted the \"SR foot\" structure that traversed the gap between the SR and the T-tubular membrane. Ca2+ channels, also called dihydropyridine receptors (DHPRs), were located in the T-tubular membrane at the triadic junction and shown to be essential for EC coupling. There was a precise relationship between the two channels. Four DHPRs, organized as tetrads, were superimposed on alternate RyRs. This structure was consistent with the proposal that EC coupling was mediated via a movement of intramembrane charge in the T-tubular system. The speculation was that the DHPR acted as a voltage sensor transferring information to the RyRs of the SR by protein-protein interaction causing the release of Ca2+ from the SR. A great deal of progress was made by 1988 toward understanding EC coupling. However, the ultimate question of how voltage-sensing is coupled to opening of the SR Ca2+ release channel remains unresolved.
摘要：
骨骼肌中的兴奋-收缩（EC）耦合表达是在1952年创造的（1）。该术语狭义地发展为仅包括三联体的过程，该过程在横管（T管）膜的去极化和肌浆网（SR）的Ca2释放之间进行干预。从1970年到1988年，阐明了EC耦合的基础。激活过程中释放Ca2的通道通过其与植物杀虫剂ryanodine的特异性结合而位于SR中。该通道被称为ryanodine受体(RyR)。RyR包含四个亚基，它们一起构成了穿越SR和T管膜之间间隙的“SR脚”结构。Ca2+通道,也称为二氢吡啶受体（DHPR），位于三元交界处的T形管膜中，对EC耦合至关重要。这两个渠道之间存在精确的关系。四个DHPR,组织为四分体，叠加在备用RyRs上。该结构与通过T管系统中膜内电荷的运动介导EC耦合的提议一致。推测DHPR充当电压传感器，通过蛋白质-蛋白质相互作用将信息传递到SR的RyRs，从而导致Ca2从SR释放。到1988年，在理解EC耦合方面取得了很大进展。然而,电压感测如何耦合到SRCa2+释放通道的打开的最终问题仍未解决。
