Calcium influx from the extracellular space promotes NADH hyperoxidation and electrical dysfunction after anoxia in hippocampal slices

Miguel A. Pérez-Pinzón, Patricia L. Mumford, Verónica Carranza, Thomas J. Sick

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

A characteristic event during reperfusion after cerebral ischemia in vivo, and reoxygenation after anoxia in vitro, is hyperoxidation of the electron carriers of the mitochondrial respiratory chain. Current studies have tested the hypothesis that there is a relation among calcium molecules derived from extracellular sources, mitochondrial hyperoxidation, and electrical recovery after anoxia in hippocampal slices. Rat hippocampal slices were superfused with artificial cerebrospinal fluids (ACSF) containing calcium chloride (CaCl2) in concentrations of: 0.5, 1, 2, and 4 mmol/L. Slices were made anoxic and then allowed to recover for 60 minutes. Reduction-oxidation shifts of NADH were measured by rapid-scanning spectrofluorometry. Synaptic activity was indicated by population spike amplitudes in the CA1 pyramidal cell subfield of the hippocampus in response to stimulation of the Schaffer collaterals. Low calcium ACSF concentrations ameliorated NADH hyperoxidation and improved synaptic transmission recovery after anoxia. High calcium ACSF concentrations had opposite effects. These data suggest a link between mitochondrial hyperoxidation and electrical recovery after postanoxia reoxygenation and support the hypothesis that cytosolic calcium overload promotes mitochondrial hyperoxidation and limits electrical recovery.

Original languageEnglish (US)
Pages (from-to)215-221
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Volume18
Issue number2
DOIs
StatePublished - Feb 1998

Keywords

  • Electron carriers
  • Evoked potentials
  • Ischemia
  • Mitochondria
  • NMDA
  • Oxidative damage
  • Permeability transition

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Endocrinology, Diabetes and Metabolism

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