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Mechanisms underlying InsP₃-evoked global Ca²⁺ signals in mouse pancreatic acinar cells

Kevin E. Fogarty *, Jackie F. Kidd, Dick A. Tuft * and Peter Thorn

1. In secretory epithelial cells, complex patterns of Ca²⁺ signals regulate physiological processes. How these patterns are generated is still not fully understood. In particular, the basis of global Ca²⁺ waves is not clear.

2. We have studied regional differences in InsP₃-evoked Ca²⁺ release in single mouse pancreatic acinar cells, using high-speed (~90 frames s^-1), high-sensitivity Ca²⁺ imaging combined with rapid (10 ms) spot photolysis (2 µm diameter) of caged InsP₃. Within a single region we measured Ca²⁺ response latency and rate of rise to construct an InsP₃ dose-response relationship.

3. Spot InsP₃ liberation in the secretory pole region consistently elicited a dose-dependent, rapid release of Ca²⁺.

4. Spot InsP₃ liberation in the basal pole region of ~50 % of cells elicited a similar dose-response relationship but with a lower apparent InsP₃ affinity than in the secretory pole. In the other cells, basal pole InsP₃ liberation did not elicit active Ca²⁺ release, even at the highest stimulus intensities we employed, although these same cells did respond when the stimulus spot was moved to different regions.

5. We conclude that in the basal pole active sites of rapid Ca²⁺ release have a lower functional affinity for InsP₃ than those in the secretory pole and are spread out in discrete sites across the basal pole. These properties explain the propagation of Ca²⁺ waves across the basal pole that are only observed at higher stimulus levels.

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