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A Model of Calcium Waves in Pancreatic and Parotid Acinar Cells

J. Sneyd ^*, K. Tsaneva-Atanasova ^*, J. I. E. Bruce , S. V. Straub , D. R. Giovannucci  and D. I. Yule 

^* Department of Mathematics, University of Auckland, Auckland, New Zealand; Department of Pharmacology and Physiology, University of Rochester, Rochester, New York; and Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo, Ohio

Correspondence: Address reprint requests to J. Sneyd, E-mail: sneyd{at}math.auckland.ac.nz.

We construct a mathematical model of Ca²⁺ wave propagation in pancreatic and parotid acinar cells. Ca²⁺ release is via inositol trisphosphate receptors and ryanodine receptors that are distributed heterogeneously through the cell. The apical and basal regions are separated by a region containing the mitochondria. In response to a whole-cell, homogeneous application of inositol trisphosphate (IP₃), the model predicts that 1), at lower concentrations of IP₃, the intracellular waves in pancreatic cells begin in the apical region and are actively propagated across the basal region by Ca²⁺ release through ryanodine receptors; 2), at higher [IP₃], the waves in pancreatic and parotid cells are not true waves but rather apparent waves, formed as the result of sequential activation of inositol trisphosphate receptors in the apical and basal regions; 3), the differences in wave propagation in pancreatic and parotid cells can be explained in part by differences in inositol trisphosphate receptor density; 4), in pancreatic cells, increased Ca²⁺ uptake by the mitochondria is capable of restricting Ca²⁺ responses to the apical region, but that this happens only for a relatively narrow range of [IP₃]; and 5), at higher [IP₃], the apical and basal regions of the cell act as coupled Ca²⁺ oscillators, with the basal region partially entrained to the apical region.

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