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 stria tum of rats during ischaemia was examined by perfusion with Ca2+-free medium and treatment with the nitric oxide synthase inhibitor, NG-nitr o-L-arginine methyl ester (L-NAME). Male Wistar rats were subjected to 30 min ischaemia using the 4-vessel occlusion model or high K+-depola rization. Extracellular glutamate and aspartate were monitored by in v ivo microdialysis. Perfusion with Ca2+-free medium and systemic admini stration 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 s uggest that the extracellular glutamate and aspartate originates from a Ca2+-independent pool during forebrain ischaemia and is not modulate d by nitric oxide. In high K+-depolarization the accumulated glutamate may arise, at least in part, from enhanced vesicular release and is m odulated by nitric oxide.