Ca2+ signalling between single L-type Ca2+ channels and ryanodine receptors in heart cells

Shi-Qiang Wang, Long-Sheng Song, Edward G. Lakatta and Heping Cheng ()
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Shi-Qiang Wang: Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health
Long-Sheng Song: Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health
Edward G. Lakatta: Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health
Heping Cheng: Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health

Nature, 2001, vol. 410, issue 6828, 592-596

Abstract: Abstract Ca2+-induced Ca2+ release is a general mechanism that most cells use to amplify Ca2+ signals1,2,3,4,5. In heart cells, this mechanism is operated between voltage-gated L-type Ca2+ channels (LCCs) in the plasma membrane and Ca2+ release channels, commonly known as ryanodine receptors, in the sarcoplasmic reticulum3,4,5. The Ca2+ influx through LCCs traverses a cleft of roughly 12 nm formed by the cell surface and the sarcoplasmic reticulum membrane, and activates adjacent ryanodine receptors to release Ca2+ in the form of Ca2+ sparks6. Here we determine the kinetics, fidelity and stoichiometry of coupling between LCCs and ryanodine receptors. We show that the local Ca2+ signal produced by a single opening of an LCC, named a ‘Ca2+ sparklet’, can trigger about 4–6 ryanodine receptors to generate a Ca2+ spark. The coupling between LCCs and ryanodine receptors is stochastic, as judged by the exponential distribution of the coupling latency. The fraction of sparklets that successfully triggers a spark is less than unity and declines in a use-dependent manner. This optical analysis of single-channel communication affords a powerful means for elucidating Ca2+-signalling mechanisms at the molecular level.

Date: 2001
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DOI: 10.1038/35069083

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