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Ca²⁺ Signaling in Mouse Pancreatic Polypeptide Cells¹

Department of Medical Cell Biology, Uppsala University, SE-751 23 Uppsala, Sweden

Address all correspondence and requests for reprints to: Erik Gylfe, Department of Medical Cell Biology, Biomedicum, Box 571, SE-751 23 Uppsala, Sweden. E-mail: erik.gylfe{at}medcellbiol.uu.se

Ca²⁺signaling was studied in pancreatic polypeptide (PP)-secreting cells isolated from mouse islets of Langerhans. After measuring the cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i), the cells were identified by immunocytochemistry. Most PP-cells reacted to carbachol and epinephrine with prompt and reversible elevation of [Ca²⁺]_i, often manifested as slow oscillations. The carbachol effect was muscarinic, because it was inhibited by atropine. ß-adrenergic elevation of cAMP explains the epinephrine stimulation, which was mimicked by an activator of adenylate cyclase and blocked by an inhibitor of protein kinase A. The responses to carbachol and epinephrine apparently involve depolarization with opening of voltage-dependent Ca²⁺ channels, because the effects were prevented by the Ca²⁺ channel antagonist methoxyverapamil and by diazoxide, which activates ATP-dependent K⁺ (K_ATP) channels. Being equipped with K_ATP channels, the PP-cells often responded to tolbutamide or high concentrations of glucose with elevation of [Ca²⁺]_i. Somatostatin reversed the [Ca²⁺]_i elevation obtained by carbachol, epinephrine, tolbutamide, and glucose. These preliminary studies support the idea that glucose has a direct stimulatory effect on the PP-cells, which can be masked by locally released somatostatin. Expressing both K_ATP channels and voltage-dependent Ca²⁺ channels, the PP-cells share fundamental regulatory mechanisms with other types of islet cells.

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