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* Department of Physiology, Medical School of Xi'an Jiaotong University, Xi'an 710061, China; Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; and National Laboratory of Biomembrane and Membrane Biotechnology, College of Life Science, Peking University, Beijing, China
Correspondence: Address reprint requests to Heping Cheng, PhD, Laboratory of Cardiovascular Science, National Institute on Aging, NIH, 5600 Nathan Shock Dr., Baltimore, MD 21224. Tel.: 410-558-8634; Fax: 410-558-8150; E-mail: chengp{at}grc.nia.nih.gov.
Ca2+ sparks are the elementary release events in many types of cells. Here we present a morphometric analysis of Ca2+ sparks (i.e., amplitude and kinetic parameters) using an approach that minimizes the confounding factor of the detection of out-of-focus events. By activation and visualization of Ca2+ sparks from Ca2+ release units under loose-seal patch-clamp conditions, we found that the amplitude and rising rate of in-focus sparks exhibited a broad modal distribution, whereas spark rise time and spatial width appeared to be stereotyped. Spark morphometrics were constant irrespective of the latency of spark production and the time-dependent L-type Ca2+ channel activation. Polymorphism of Ca2+ sparks in terms of variable amplitude and rising rate was evident for events from the same release units, and intra- and interrelease unit variability contributed equally to the overall variability. The rising rate, a reporter of the underlying Ca2+ release flux, displayed a strong positive correlation with spark amplitude, but a negative correlation with spark rise time, an index of Ca2+ release duration. On the basis of Ca2+ spark morphometrics measured here, we suggested a model in which cohorts of variable number of ryanodine receptors are activated in the genesis of Ca2+ sparks, and the ensuing negative feedback overrides the regenerative Ca2+-induced Ca2+ release to extinguish the ongoing Ca2+ spark.
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