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Filtering of Calcium Transients by the Endoplasmic Reticulum in Pancreatic ß-Cells

Richard Bertram ^* and Arthur Sherman 

^* Department of Mathematics and Institute of Molecular Biophysics, Florida State University, Tallahassee, Florida; and Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland

Correspondence: Address reprint requests to Richard Bertram, Tel.: 850-644-7195; E-mail: bertram{at}math.fsu.edu.

Calcium handling in pancreatic ß-cells is important for intracellular signaling, the control of electrical activity, and insulin secretion. The endoplasmic reticulum (ER) is a key organelle involved in the storage and release of intracellular Ca²⁺. Using mathematical modeling, we analyze the filtering properties of the ER and clarify the dual role that it plays as both a Ca²⁺ source and a Ca²⁺ sink. We demonstrate that recent time-dependent data on the free Ca²⁺ concentration in pancreatic islets and ß-cell clusters can be explained with a model that uses a passive ER that takes up Ca²⁺ when the cell is depolarized and the cytosolic Ca²⁺ concentration is elevated, and releases Ca²⁺ when the cell is repolarized and the cytosolic Ca²⁺ is at a lower concentration. We find that Ca²⁺-induced Ca²⁺ release is not necessary to explain the data, and indeed the model is inconsistent with the data if Ca²⁺-induced Ca²⁺ release is a dominating factor. Finally, we show that a three-compartment model that includes a subspace compartment between the ER and the plasma membrane provides the best agreement with the experimental Ca²⁺ data.

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