GLUTAMATE‐INDUCED CALCIUM LOADS: EFFECTS ON ENERGY METABOLISM AND NEURONAL VIABILITY

Stanley A Thayer, Guang Jian Wang

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

1. Glutamate‐induced increases in intracellular free Ca2+ concentration ([Ca2+]i) were recorded from cultured rat hippocampal neurons with single cell microfluorometry. The [Ca2+]i increase did not correlate with glutamate‐induced cell death, consistent with the idea that Ca2+ accumulates in an intracellular store, and that loading this store might be toxic. 2. Glutamate‐induced Ca2+ loads were buffered by a low‐affinity, high‐capacity process that was inhibited by the mitochondrial uncoupling agent FCCP and modulated by intracellular Na+. 3. Glutamate‐induced Ca2+ loads also produced an intracellular acidification. The acidification was prevented by the metabolic inhibitor 2‐deoxyglucose, mimicked by Ba2+, and inhibited by microinjection of ruthenium red. 4. These data are consistent with the hypothesis that mitochondria sequester glutamate‐induced Ca2+ loads producing a metabolic acidosis; metabolic stress may contribute to glutamate‐induced neuronal death.

Original languageEnglish (US)
Pages (from-to)303-304
Number of pages2
JournalClinical and Experimental Pharmacology and Physiology
Volume22
Issue number4
DOIs
StatePublished - Apr 1995

Keywords

  • glutamate
  • intracellular calcium
  • intracellular pH
  • mitochondria
  • neurotoxicity.

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