Synchronization of pancreatic beta-cell rhythmicity after glucagon induction of Ca2+ transients

Cell Calcium. 2003 Jul;34(1):49-53. doi: 10.1016/s0143-4160(03)00021-6.

Abstract

Pancreatic beta-cells are biological oscillators requiring a coupling force for the synchronization of the cytoplasmic Ca(2+) oscillations responsible for pulsatile insulin release. Testing the idea that transients, superimposed on the oscillations, are important for this synchronization, the concentration of cytoplasmic Ca(2+) ([Ca(2+)](i)) was measured with ratiometric fura-2 technique in single beta-cells and small aggregates prepared from islets isolated from ob/ob-mice. Image analyses revealed asynchronous [Ca(2+)](i) oscillations in adjacent beta-cells lacking physical contact. The addition of glucagon stimulated the firing of [Ca(2+)](i) transients, which appeared in synchrony in adjacent beta-cells. Moreover, the presence of glucagon promoted synchronization of the [Ca(2+)](i) oscillations in beta-cells separated by a distance <100 microm but not in those >200 microm apart. The results support the proposal that the repolarizing effect of [Ca(2+)](i) transients provides a coupling force for co-ordinating the pulses of insulin release generated by pancreatic beta-cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology*
  • Cell Communication / drug effects
  • Cell Communication / physiology*
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Cells, Cultured
  • Fura-2
  • Glucagon / metabolism*
  • Glucagon / pharmacology
  • Islets of Langerhans / cytology
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Mice
  • Mice, Obese
  • Periodicity*

Substances

  • Glucagon
  • Calcium
  • Fura-2