Abstract
Pancreatic islets contain and release high concentrations of GABA. GABA is thought to play a paracrine role in beta-cells. Searching for a paracrine function of GABA in neoplastic beta-cells we performed patch-clamp studies in isolated human insulinoma cells. We show that human insulinoma cells can express functional GABAA receptors. Activation of GABAA receptors caused a reversible membrane depolarization in a subgroup of insulinoma cells. Membrane depolarization resulted in transmembraneous calcium influx through voltage-gated calcium channels and stimulation of insulin secretion. Insulin secretion was increased by the GABAA receptor agonist muscimol (50 microM) by about 280%. Thus, GABAA receptors can be expressed in human insulinoma cells and can regulate their insulin release.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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Cadmium Chloride / pharmacology
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Calcium Channel Blockers / pharmacology
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Calcium Channels / physiology
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Female
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Humans
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Insulin / metabolism
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Insulin Secretion
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Insulinoma / pathology
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Insulinoma / physiopathology*
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Insulinoma / surgery
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Isradipine / pharmacology
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Middle Aged
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Muscimol / pharmacology
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Pancreatic Neoplasms / pathology
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Pancreatic Neoplasms / physiopathology*
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Pancreatic Neoplasms / surgery
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Patch-Clamp Techniques
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Picrotoxin / pharmacology
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Receptors, GABA-A / physiology*
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Tumor Cells, Cultured
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gamma-Aminobutyric Acid / pharmacology
Substances
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Calcium Channel Blockers
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Calcium Channels
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Insulin
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Receptors, GABA-A
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Picrotoxin
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Muscimol
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gamma-Aminobutyric Acid
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Cadmium Chloride
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Isradipine