L-NAME MODULATES GLUTAMATE ACCUMULATION INDUCED BY K+-DEPOLARIZATION BUT NOT BY FOREBRAIN ISCHEMIA IN THE RAT STRIATUM

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.