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Ca²⁺-Induced Ca²⁺ Release in the Pancreatic ß-Cell: Direct Evidence of Endoplasmic Reticulum Ca²⁺ Release

Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York 14642

Address all correspondence and requests for reprints to: Patricia M. Hinkle, Ph.D., University of Rochester Medical Center, Box 711, 601 Elmwood Avenue, Rochester, New York 14642. E-mail: patricia_hinkle{at}urmc.rochester.edu.

The role of the Ca²⁺-induced Ca²⁺ release channel (ryanodine receptor) in MIN6 pancreatic ß-cells was investigated. An endoplasmic reticulum (ER)-targeted "cameleon" was used to report lumenal free Ca²⁺. Depolarization of MIN6 cells with KCl led to release of Ca²⁺ from the ER. This ER Ca²⁺ release was mimicked by treatment with the ryanodine receptor agonists caffeine and 4-chloro-m-cresol, reversed by voltage-gated Ca²⁺ channel antagonists and blocked by treatment with antagonistic concentrations of ryanodine. The depolarization-induced rise in cytoplasmic Ca²⁺ was also inhibited by ryanodine, which did not alter voltage-gated Ca²⁺ channel activation. Both ER and cytoplasmic Ca²⁺ changes induced by depolarization occurred in a dose-dependent manner. Glucose caused a delayed rise in cytoplasmic Ca²⁺ but no detectable change in ER Ca²⁺. Carbamyl choline caused ER Ca²⁺ release, a response that was not altered by ryanodine. Taken together, these results provide strong evidence that Ca²⁺-induced Ca²⁺ release augments cytoplasmic Ca²⁺ signals in pancreatic ß-cells.

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