Calcium dependence of hypoosmotically induced potassium release in cultured astrocytes

Alex S. Bender, Michael D Norenberg

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

A major mechanism in cell volume regulation after hypoosmotic stress is K+ release. Our studies show that in astrocytes, K+ release during hypoosmotic stress is a Ca2+-dependent process. Agents that increase intracellular Ca2+, such as ionomycin and ouabain, potentiated hypoosmotically stimulated K+ release, while compounds that block Ca2+ entry during hypoosmotic stress, such as nimodipine, bepridil, and MK-801, inhibited hypoosmotically stimulated K+ release. Similarly, chelation of intracellular Ca2+ blocked hypoosmotically induced K+ release. Caffeine and U-73122 also inhibited K+ efflux under hypoosmotic conditions, suggesting that intracellular Ca2+ release from Ca2+-induced Ca2+ release stores and inositol trisphosphate-sensitive intracellular Ca2+ stores play a role in the mechanism of K+ release. Blocking the activity of calmodulin, and of CaM kinase, attenuated hypoosmotically induced K+ release. Our findings indicate that entry of extracellular Ca2+ and Ca2+ release from intracellular stores play a key role in the activation of K+ release under hypoosmotic conditions and thus in cell volume regulation.

Original languageEnglish
Pages (from-to)4237-4243
Number of pages7
JournalJournal of Neuroscience
Volume14
Issue number7
StatePublished - Jul 1 1994

Fingerprint

Cell Size
Astrocytes
Potassium
Bepridil
Calcium
Nimodipine
Calcium-Calmodulin-Dependent Protein Kinases
Ionomycin
Dizocilpine Maleate
Inositol
Ouabain
Caffeine
1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione

Keywords

  • astrocytes
  • calcium
  • hypoosmotic stress
  • potassium
  • volume regulation

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Calcium dependence of hypoosmotically induced potassium release in cultured astrocytes. / Bender, Alex S.; Norenberg, Michael D.

In: Journal of Neuroscience, Vol. 14, No. 7, 01.07.1994, p. 4237-4243.

Research output: Contribution to journalArticle

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