A univariate model of calcium release in the dyadic cleft of cardiac myocytes.

Local calcium sparks in the dyadic cleft of cardiac myocytes are triggered by calcium influxes via L-type calcium channels (LCCs) located on the transverse tubule (TT) membrane, and subsequently controlled by the regeneration of ryanodine receptors (RyRs) on the sarcoplasmic reticulum (SR). Calcium released from SR channels is known to be responsible for the sparks. Therefore, the activities of RyRs provide straightforward indication to the calcium concentration alteration. A method to study calcium signaling by analyzing RyR-gating statistics is described in the present study. Here we propose a univariate model with a simplified geometry of the dyadic cleft, which specifies the spatial localization of LCCs and RyRs to monitor the activity changes of RyRs. This model is used to explore two crucial aspects of local calcium signaling: the first is to disclose the tight control of calcium influxes via LCCs, and the second is to reveal the interactional impact of the self-regenerative RyRs. Patterns of active RyRs are rendered through numerous computational simulation experiments, manipulating the state initialization and the spatial localization of LCCs and RyRs to observe gating transition of RyRs.