ArticleThe Journal of physiology2004
Capacitance measurements of exocytosis in mouse pancreatic alpha-, beta- and delta-cells within intact islets of Langerhans.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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83 citing papers in PubMed, 158 citations in OpenAlex.
- Antecedent hypoglycaemia impairs glucagon secretion by enhancing somatostatin-mediated negative feedback control.Nature metabolism · 2026Article
- The Amount of Releasable Insulin Depends on Continuous Oxidative Phosphorylation.Function (Oxford, England) · 2025Article
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- α-cell electrophysiology and the regulation of glucagon secretion.The Journal of endocrinology · 2023Review
- Loss of tetraspanin-7 expression reduces pancreatic β-cell exocytosis CaDiabetic medicine : a journal of the British Diabetic Association · 2022Article
- The changing view of insulin granule mobility: From conveyor belt to signaling hub.Frontiers in endocrinology · 2022Review
- Somatostatin receptors in congenital hyperinsulinism: Biology to bedside.Frontiers in endocrinology · 2022Review
- Dynamin deficiency causes insulin secretion failure and hyperglycemia.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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- Drp1-dependent mitochondrial fission in cardiovascular disease.Acta pharmacologica Sinica · 2021Review
- CaChannels (Austin, Tex.) · 2020Review
- Glucokinase intrinsically regulates glucose sensing and glucagon secretion in pancreatic alpha cells.Scientific reports · 2020Article
- 'Resistance is futile?' - paradoxical inhibitory effects of KThe Journal of physiology · 2020Review
- Cellular and systemic mechanisms for glucose sensing and homeostasis.Pflugers Archiv : European journal of physiology · 2020Review
- Exocytotic fusion pore under stress.Cell stress · 2020Review
- Calcium Oscillations in Pancreatic α-cells Rely on Noise and ATP-Driven Changes in Membrane Electrical Activity.Frontiers in physiology · 2020Article
- Glucose stimulates somatostatin secretion in pancreatic δ-cells by cAMP-dependent intracellular CaThe Journal of general physiology · 2019Article
- Cyclic AMP links glucose stimulation to somatostatin secretion in δ-cells.The Journal of general physiology · 2019Article
- Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Capacitance measurements of exocytosis were applied to functionally identified alpha-, beta- and delta-cells in intact mouse pancreatic islets. The maximum rate of capacitance increase in beta-cells during a depolarization to 0 mV was equivalent to 14 granules s(-1), <5% of that observed in isolated beta-cells. Beta-cell secretion exhibited bell-shaped voltage dependence and peaked at +20 mV. At physiological membrane potentials (up to approximately -20 mV) the maximum rate of release was approximately 4 granules s(-1). Both exocytosis (measured by capacitance measurements) and insulin release (detected by radioimmunoassay) were strongly inhibited by the L-type Ca(2+) channel blocker nifedipine (25 microm) but only marginally (<20%) affected by the R-type Ca(2+) channel blocker SNX482 (100 nm). Exocytosis in the glucagon-producing alpha-cells peaked at +20 mV. The capacitance increases elicited by pulses to 0 mV exhibited biphasic kinetics and consisted of an initial transient (150 granules s(-1)) and a sustained late component (30 granules s(-1)). Whereas addition of the N-type Ca(2+) channel blocker omega-conotoxin GVIA (0.1 microm) inhibited glucagon secretion measured in the presence of 1 mm glucose to the same extent as an elevation of glucose to 20 mm, the L-type Ca(2+) channel blocker nifedipine (25 microm) had no effect. Thus, glucagon release during hyperglycaemic conditions depends principally on Ca(2+)-influx through N-type rather than L-type Ca(2+) channels. Exocytosis in the somatostatin-secreting delta-cells likewise exhibited two kinetically separable phases of capacitance increase and consisted of an early rapid (600 granules s(-1)) component followed by a sustained slower (60 granules s(-1)) component. We conclude that (1) capacitance measurements in intact pancreatic islets are feasible; (2) exocytosis measured in beta-cells in situ is significantly slower than that of isolated cells; and (3) the different types of islet cells exhibit distinct exocytotic features.
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