Voltage-dependent intracellular calcium release from mouse islets stimulated by glucose

• Published in: The Journal of biological chemistry Vol. 268; no. 14; pp. 9953 - 9956
• Main Authors: Roe, M.W., Lancaster, M.E., Mertz, R.J., Worley, J.F., Dukes, I.D.
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Elsevier Inc 15-05-1993; American Society for Biochemistry and Molecular Biology
• Subjects: Animals; Biological and medical sciences; Caffeine - pharmacology; Calcium - metabolism; Calcium Channels - physiology; Cell physiology; Cells, Cultured; Egtazic Acid - pharmacology; Fundamental and applied biological sciences. Psychology; Fura-2; Glucose - pharmacology; Islets of Langerhans - drug effects; Islets of Langerhans - metabolism; Islets of Langerhans - physiology; Kinetics; Membrane Potentials - drug effects; Mice; Mice, Inbred C57BL; Molecular and cellular biology; Potassium Chloride - pharmacology; Ryanodine - pharmacology; Secretion. Exocytosis; Tetrodotoxin - pharmacology; Depolarization; Vertebrata; Mammalia; Calcium; Mouse; Secretion; Rodentia; Langerhans islet; Stimulation; Glucose; Fluorescence spectrometry
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/S0021-9258(18)82156-1

Glucose-activated beta-cell insulin secretion depends upon elevation of intracellular calcium concentration, [Ca2+]i, which is thought to arise from Ca2+ influx through voltage-dependent calcium channels. Using fura-2-loaded mouse islets, we demonstrate, in fact, that the major component of the glucose-activated [Ca2+]i rise represents voltage-dependent intracellular Ca2+ release. Furthermore, the Ca2+ release pool possesses a novel pharmacology in that it is caffeine-sensitive but ryanodine-insensitive. In the absence of external Ca2+, glucose still caused intracellular Ca2+ release, an effect blockable by tetrodotoxin. However, depolarization of the islet with KCl in low Ca(2+)-containing solutions induced intracellular Ca2+ release, which was resistant to tetrodotoxin. We conclude that glucose release of intracellular Ca2+ is dependent upon depolarization alone, possibly through increasing inositol 1,4,5-trisphosphate production.