期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：44
页码：15793-15798
DOI：10.1073/pnas.0403485101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Store-operated Ca2+ entry (SOCE) occurs in diverse cell types in response to depletion of Ca2+ within the endoplasmic/sarcoplasmic reticulum and functions both to refill these stores and to shape cytoplasmic Ca2+ transients. Here we report that in addition to conventional SOCE, skeletal myotubes display a physiological mechanism that we term excitation-coupled Ca2+ entry (ECCE). ECCE is rapidly initiated by membrane depolarization. Like excitation-contraction coupling, ECCE is absent in both dyspedic myotubes that lack the skeletal muscle-type ryanodine receptor 1 and dysgenic myotubes that lack the dihydropyridine receptor (DHPR), and is independent of the DHPR L-type Ca2+ current. Unlike classic SOCE, ECCE does not depend on sarcoplasmic reticulum Ca2+ release. Indeed, ECCE produces a large Ca2+ entry in response to physiological stimuli that do not produce substantial store depletion and depends on interactions among three different Ca2+ channels: the DHPR, ryanodine receptor 1, and a Ca2+ entry channel with properties corresponding to those of store-operated Ca2+ channels. ECCE may provide a fundamental means to rapidly maintain Ca2+ stores and control important aspects of Ca2+ signaling in both muscle and nonmuscle cells.
