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

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
Publication statusPublished - Jun 6 1994

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

l-NAME modulates glutamate accumulation induced by K+-depolarization but not by forebrain ischaemia in the rat striatum. / Ghribi, Othman; Callebert, Jacques; Plotkine, Michel; Boulu, Roger G.

In: Neuroscience Letters, Vol. 174, No. 1, 06.06.1994, p. 34-38.

Research output: Contribution to journalArticle