Didier X.P. Brochet

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RATIONALE Sinoatrial node cells (SANCs) generate local, subsarcolemmal Ca(2+) releases (LCRs) from sarcoplasmic reticulum (SR) during late diastolic depolarization. LCRs activate an inward Na(+)-Ca(2+) exchange current (I(NCX)), which accelerates diastolic depolarization rate, prompting the next action potential (AP). The LCR period, ie, a delay between(More)
Ca2+ ions passing through a single or a cluster of Ca2+-permeable channels create microscopic, short-lived Ca2+ gradients that constitute the building blocks of cellular Ca2+ signaling. Over the last decade, imaging microdomain Ca2+ in muscle cells has unveiled the exquisite spatial and temporal architecture of intracellular Ca2+ dynamics and has reshaped(More)
RATIONALE In cardiac myocytes, "Ca(2+) sparks" represent the stereotyped elemental unit of Ca(2+) release arising from activation of large arrays of ryanodine receptors (RyRs), whereas "Ca(2+) blinks" represent the reciprocal Ca(2+) depletion signal produced in the terminal cisterns of the junctional sarcoplasmic reticulum. Emerging evidence, however,(More)
Elemental calcium signals from RYR arrays operating in cardiac myocytes have been extensively characterized with ever-improving optical methods and other innovative techniques. However, the exact nature of elemental calcium signals in terms of RYR gating in situ remains an enigma. Here, we synthesize insights gleaned from recent developments in(More)
Ca(2+) release events underlie global Ca(2+) signaling yet they are regulated by local, subcellular signaling features. Here we review the latest developments of different elementary Ca(2+) release features that include Ca(2+) sparks, Ca(2+) blinks (the corresponding depletion of Ca(2+) in the sarcoplasmic reticulum (SR) during a spark) and the recently(More)
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