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Mitochondria possess a remarkable ability to rapidly accumulate and sequester Ca 2+ . One of the mechanisms responsible for this ability is believed to be the rapid mode (RaM) of Ca 2+  uptake. Despite the existence of many models of mitochondrial Ca 2+  dynamics, very few consider RaM as a potential mechanism that regulates mitochondrial Ca 2+  dynamics. To fill this gap, a novel mathematical model of the RaM mechanism is developed herein. The model is able to simulate the available experimental data of rapid Ca 2+  uptake in isolated mitochondria from both chicken heart and rat liver tissues with good fidelity. The mechanism is based on Ca 2+  binding to an external trigger site(s) and initiating a brief transient of high Ca 2+  conductivity. It then quickly switches to an inhibited, zero-conductive state until the external Ca 2+  level is dropped below a critical value (∼100–150 nM). RaM's Ca 2+ - and time-dependent properties make it a unique Ca 2+  transporter that may be an important means by which mitochondria take up Ca 2+   in situ  and help enable mitochondria to decode cytosolic Ca 2+  signals. Integrating the developed RaM model into existing models of mitochondrial Ca 2+  dynamics will help elucidate the physiological role that this unique mechanism plays in mitochondrial Ca 2+ -homeostasis and bioenergetics.

A Minimal Model for the Mitochondrial Rapid Mode of Ca2+ Uptake Mechanism