Ca2+ signaling regulated by an ATP-dependent autocrine mechanism in astrocytes

Neuroreport. 2001 Aug 28;12(12):2619-22. doi: 10.1097/00001756-200108280-00007.

Abstract

Although the mechanisms of Ca2+ wave propagation in astrocytes induced by mechanical stimulation have been well studied, it is still not known how the [Ca2+]i increases in the stimulated cells. Here, we have analyzed the mechanisms of [Ca2+]i increase in single, isolated astrocytes. Our results showed that there was an autocrine mechanism of Ca2+ regulation mediated by ATP in mechanically stimulated astrocytes. This autocrine mechanism induced the activation of phospholipase C via a G-protein, resulting in Ca2+ release from intracellular Ca2+ stores. A second pathway mediating a [Ca2+]i increase was via a Ca2+ influx from the extracellular space, which, interestingly, suppressed an intracellular Ca2+ oscillation. These two different Ca2+ cascades are involved in signal transduction and may function separately during intercellular communication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Animals
  • Astrocytes / cytology
  • Astrocytes / drug effects
  • Astrocytes / metabolism*
  • Autocrine Communication / drug effects
  • Autocrine Communication / physiology*
  • Calcium / metabolism
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology*
  • Cells, Cultured
  • Estrenes / pharmacology
  • GTP-Binding Proteins / metabolism
  • Intracellular Fluid / metabolism
  • Phosphodiesterase Inhibitors / pharmacology
  • Physical Stimulation
  • Purinergic P2 Receptor Antagonists
  • Pyrrolidinones / pharmacology
  • Rats
  • Rats, Wistar
  • Suramin / pharmacology
  • Type C Phospholipases / antagonists & inhibitors
  • Type C Phospholipases / metabolism

Substances

  • Estrenes
  • Phosphodiesterase Inhibitors
  • Purinergic P2 Receptor Antagonists
  • Pyrrolidinones
  • 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione
  • Suramin
  • Adenosine Triphosphate
  • Type C Phospholipases
  • GTP-Binding Proteins
  • Calcium