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.
- Forebrain ischaemia
- Nitric oxide
ASJC Scopus subject areas
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.
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