l-NAME modulates glutamate accumulation induced by K+-depolarization but not by forebrain ischaemia in the rat striatum

Othman Ghribi, Jacques Callebert, Michel Plotkine, Roger G. Boulu

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

The accumulation of extracellular glutamate and aspartate in the striatum of rats during ischaemia was examined by perfusion with Ca2+-free medium and treatment with the nitric oxide synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME). Male Wistar rats were subjected to 30 min ischaemia using the 4-vessel occlusion model or high K+-depolarization. Extracellular glutamate and aspartate were monitored by in vivo microdialysis. Perfusion with Ca2+-free medium and systemic administration or local perfusion of l-NAME reduced the K+-evoked glutamate accumulation but not the ischaemia-induced glutamate accumulation. The aspartate concentration was unaffected in both conditions. Our data suggest that the extracellular glutamate and aspartate originates from a Ca2+-independent pool during forebrain ischaemia and is not modulated by nitric oxide. In high K+-depolarization the accumulated glutamate may arise, at least in part, from enhanced vesicular release and is modulated by nitric oxide.

Original languageEnglish (US)
Pages (from-to)34-38
Number of pages5
JournalNeuroscience Letters
Volume174
Issue number1
DOIs
StatePublished - Jun 6 1994

Keywords

  • Ca
  • Forebrain ischaemia
  • Glutamate
  • Microdialysis
  • Nitric oxide
  • Striatum
  • l-NAME

ASJC Scopus subject areas

  • Neuroscience(all)

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