Early sodium elevations induced by combined oxygen and glucose deprivation in pyramidal cortical neurons

A. Pisani, P. Calabresi, A. Tozzi, G. Bernardi, T. Knopfel

Research output: Contribution to journalArticlepeer-review

Abstract

We investigated the effects of oxygen (O2)/glucose deprivation on intracellular sodium concentration ([Na+](i)) of cortical pyramidal cells in a slice preparation of rat frontal cortex. Intracellular recordings were combined with microfluorometric measurements of [Na+](i) using the Na+-sensitive dye sodium-binding benzofuran isophthalate (SBFI). Deprivation of O2/glucose caused an initial membrane hyperpolarization that was followed by a slowly developing large depolarization. Levels of [Na+](i) started to increase significantly during the phase of membrane hyperpolarization. Neither tetrodotoxin, a combination of ionotropic and metabotropic glutamate receptor antagonists (D-amino-phosphonovalerate, 6-cyano-7-nitroquinoxaline-2,3-dione plus S-methyl-4-carboxyphenylglycine) nor bepridil, an inhibitor of the Na+/Ca2+-exchanger, affected these responses to O2/ glucose. The present results demonstrate that, in cortical neurons, O2/glucose deprivation induces an early rise in [Na+](i) which cannot be ascribed to the activity of voltage gated Na+-channels, glutamate receptors or of the Na+/Ca2+-exchanger.

Original languageEnglish
Pages (from-to)3572-3574
Number of pages3
JournalEuropean Journal of Neuroscience
Volume10
Issue number11
DOIs
Publication statusPublished - 1998

Keywords

  • Electrophysiology
  • Glutamate receptors
  • Ischaemia
  • Na/Ca-exchanger
  • Optical recordings
  • Sodium channels

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Early sodium elevations induced by combined oxygen and glucose deprivation in pyramidal cortical neurons'. Together they form a unique fingerprint.

Cite this