Glassmeier G, Höpfner M, Buhr H, Lemmer K, Riecken E O, Stein H, Quabbe H J, Rancso C, Wiedenmann B, Scherübl H
Abteilung Innere Medizin/Gastroenterologie, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Germany.
Ann N Y Acad Sci. 1998 Nov 17;859:241-8. doi: 10.1111/j.1749-6632.1998.tb11138.x.
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.