The role of voltage-dependent Ca²⁺ entry for glucose generation of slow oscillations of the cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i) was evaluated in individual mouse pancreatic -cells. Like depolarization with K⁺, a rise of the glucose concentration resulted in an enhanced influx of Mn²⁺, which was inhibited by nifedipine. This antagonist of L-type Ca²⁺ channels also blocked the slow oscillations of [Ca²⁺]_i induced by glucose. The slow oscillations occurred in synchrony with variations in Mn²⁺ influx and bursts of action currents, with the elevation of [Ca²⁺]_i being proportional to the frequency of the action currents. A similar relationship was obtained when Ca²⁺ was replaced with Sr²⁺. Occasionally, the slow [Ca²⁺]_i oscillations were superimposed with pronounced spikes temporarily arresting the action currents. It is concluded that the glucose-induced slow oscillations of [Ca²⁺]_i are caused by periodic depolarization with Ca²⁺ influx through L-type channels. Ca²⁺ spiking, due to intracellular mobilization, may be important for chopping the slow oscillations of [Ca²⁺]_i into shorter ones characterizing -cells situated in pancreatic islets.

islet -cells; calcium ion entry; strontium ion; cytoplasmic calcium ion oscillations

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