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We have monitored electrical activity, voltage-gated Ca2+ currents, and exocytosis in single rat glucagon-secreting pancreatic A-cells. The A-cells were electrically excitable and generated spontaneous Na+- and Ca2+-dependent action potentials. Under basal conditions, exocytosis was tightly linked to Ca2+ influx through omega-conotoxin-GVIA-sensitive (N-type) Ca2+ channels. Stimulation of the A-cells with adrenaline (via beta-adrenergic receptors) or forskolin produced a greater than fourfold PKA-dependent potentiation of depolarization-evoked exocytosis. This enhancement of exocytosis was due to a 50% enhancement of Ca2+ influx through L-type Ca2+ channels, an effect that accounted for <30% of the total stimulatory action. The remaining 70% of the stimulation was attributable to an acceleration of granule mobilization resulting in a fivefold increase in the number of readily releasable granules near the L-type Ca2+ channels.

Original publication




Journal article


J Gen Physiol

Publication Date





217 - 228


Animals, Calcium, Calcium Channels, Cyclic AMP, Cyclic AMP-Dependent Protein Kinases, Cytoplasm, Electric Conductivity, Enzyme Activation, Epinephrine, Exocytosis, Glucagon, Glucose, Islets of Langerhans, Male, Osmolar Concentration, Rats, Rats, Inbred Lew, Receptors, Adrenergic, beta