Abstract

Oscillations in intracellular free Ca2+ concentration ([Ca2+]i) have been observed in a variety of cell types. In the present study, we constructed a mathematical model to simulate the caffeine-induced [Ca2+]i oscillations based on experimental data obtained from isolated type I horizontal cell of carp retina. The results of model analysis confirm the notion that the caffeine-induced [Ca2+]i oscillations involve a number of cytoplasmic and endoplasmic Ca2+ processes that interact with each other. Using this model, we evaluated the importance of store-operated channel (SOC) in caffeine-induced [Ca2+]i oscillations. The model suggests that store-operated Ca2+ entry (SOCE) is elicited upon depletion of the endoplasmic reticulum (ER). When the SOC conductance is set to 0, caffeine-induced [Ca2+]i oscillations are abolished, which agrees with the experimental observation that [Ca2+]i oscillations were abolished when SOC was blocked pharmacologically, verifying that SOC is necessary for sustained [Ca2+]i oscillations.

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