The foundation of excitation-contraction coupling in skeletal muscle: communication between the transverse tubules and sarcoplasmic reticulum.

IF 1.7 4区 教育学 Q2 EDUCATION, SCIENTIFIC DISCIPLINES Advances in Physiology Education Pub Date : 2024-12-01 Epub Date: 2024-08-08 DOI:10.1152/advan.00086.2024
Jack A Rall
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Abstract

The expression excitation-contraction (EC) coupling in skeletal muscle was coined in 1952 (Sandow A. Yale J Biol Med 25: 176-201, 1952). 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 the opening of the SR Ca2+ release channel remains unresolved.NEW & NOTEWORTHY The least understood part of the series of events in excitation-contraction coupling in skeletal muscle was how information was transmitted from the transverse tubules to the sarcoplasmic (SR) and how Ca2+ was released from the SR. Through an explosion of technical approaches including physiological, biochemical, structural, pharmacological, and molecular genetics, much was discovered between 1970 and 1988. By the end of 1988, the foundation of EC coupling in skeletal muscle was established.

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骨骼肌兴奋-收缩耦合的基础:横纹肌小管与肌浆网之间的沟通。
骨骼肌中的兴奋-收缩(EC)耦合这一说法诞生于 1952 年(1)。该术语狭义地演变为只包括横小管(T-tubular)膜去极化和肌浆网(SR)释放 Ca2+ 之间的三联体过程。从 1970 年到 1988 年,EC 耦合的基础被阐明。激活过程中释放 Ca2+ 的通道通过与植物杀虫剂雷诺丁的特异性结合被定位在 SR 中。这一通道被称为雷诺丁受体(RyR)。RyR 包含四个亚基,共同构成 "SR 足 "结构,穿越 SR 和 T 管膜之间的间隙。Ca2+通道,也称为二氢吡啶受体(DHPRs),位于三联体交界处的T管膜上,对心肌耦合至关重要。这两种通道之间存在着精确的关系。四个 DHPRs 以四分体的形式叠加在交替的 RyRs 上。这种结构与 EC 耦合是通过 T 管系统中的膜内电荷移动介导的这一提议相一致。根据推测,DHPR 起着电压传感器的作用,通过蛋白质与蛋白质之间的相互作用将信息传递给 SR 的 RyR,从而导致从 SR 释放 Ca2+。到 1988 年,在理解 EC 耦合方面取得了很大进展。然而,电压感应如何与 SR Ca2+ 释放通道的开启相耦合这一终极问题仍未解决。
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来源期刊
CiteScore
3.40
自引率
19.00%
发文量
100
审稿时长
>12 weeks
期刊介绍: Advances in Physiology Education promotes and disseminates educational scholarship in order to enhance teaching and learning of physiology, neuroscience and pathophysiology. The journal publishes peer-reviewed descriptions of innovations that improve teaching in the classroom and laboratory, essays on education, and review articles based on our current understanding of physiological mechanisms. Submissions that evaluate new technologies for teaching and research, and educational pedagogy, are especially welcome. The audience for the journal includes educators at all levels: K–12, undergraduate, graduate, and professional programs.
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