Ghribi O, Callebert J, Plotkine M, Boulu R G
Laboratoire de Pharmacologie, Faculté des Sciences Pharmaceutiques et Biologiques, Universitè René Descartes, Paris, France.
Neurosci Lett. 1994 Jun 6;174(1):34-8. doi: 10.1016/0304-3940(94)90112-0.
The accumulation of extracellular glutamate and aspartate in the striatum of rats during ischaemia was examined by perfusion with Ca(+)-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 Ca(2+)-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 Ca(2+)-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.
通过用无钙培养基灌注以及用一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）处理，研究了缺血期间大鼠纹状体中细胞外谷氨酸和天冬氨酸的积累情况。使用四血管闭塞模型或高钾去极化对雄性Wistar大鼠进行30分钟的缺血处理。通过体内微透析监测细胞外谷氨酸和天冬氨酸。用无钙培养基灌注以及全身性给予或局部灌注L-NAME可减少钾离子诱发的谷氨酸积累，但不能减少缺血诱导的谷氨酸积累。在两种情况下，天冬氨酸浓度均未受影响。我们的数据表明，在前脑缺血期间，细胞外谷氨酸和天冬氨酸源自不依赖钙离子的池，且不受一氧化氮的调节。在高钾去极化过程中，积累的谷氨酸可能至少部分源自囊泡释放增强，并受一氧化氮的调节。
