Gottlieb M, Domercq M, Matute C
Departamento de Neurociencias, Universidad del País Vasco, Vizcaya, Spain.
J Cereb Blood Flow Metab. 2000 Apr;20(4):678-87. doi: 10.1097/00004647-200004000-00005.
Glutamate uptake is reduced during ischemia because of perturbations of ionic gradients across neuronal and glial membranes. Using immunohistochemical and Western blot analyses, the authors examined the expression of the glutamate transporters EAAC1, GLAST, and GLT-1 in the rat hippocampus and cerebral cortex 8 hours and 1 to 28 days after transient forebrain ischemia. Densitometric analysis of immunoblots of CA1 homogenates showed a moderate increase in EAAC1 protein levels early after the insult. Consistently, it was observed that EAAC1 immunostaining in CA1 pyramidal neurons was more intense after 8 hours and 1 day of reperfusion and reduced at later postischemia stages. A similar transient increase of EAAC1 immunolabeling was detected in layer V pyramidal neurons of the cerebral cortex. In addition, the authors observed that EAAC1 also was located in oligodendroglial progenitor cells in subcortical white matter. The number of EAAC1-labeled cells in this region was increased after 3 and 28 days of reperfusion. Finally, changes in GLAST and GLT-1 expression were not observed in the CA1 region after ischemia using immunohistochemical study or immunoblotting. Enhanced expression of EAAC1 may be an adaptive response to increased levels of extracellular glutamate during ischemia.
由于跨神经元和胶质细胞膜的离子梯度紊乱，缺血期间谷氨酸摄取减少。作者使用免疫组织化学和蛋白质印迹分析，检测了短暂性前脑缺血后8小时以及1至28天大鼠海马体和大脑皮质中谷氨酸转运体EAAC1、GLAST和GLT-1的表达。对CA1匀浆免疫印迹的光密度分析显示，损伤后早期EAAC1蛋白水平适度增加。一致的是，观察到再灌注8小时和1天后，CA1锥体神经元中的EAAC1免疫染色更强，而在缺血后期则减弱。在大脑皮质V层锥体神经元中也检测到EAAC1免疫标记有类似的短暂增加。此外，作者观察到EAAC1也位于皮质下白质中的少突胶质前体细胞中。再灌注3天和28天后，该区域中EAAC1标记的细胞数量增加。最后，使用免疫组织化学研究或蛋白质印迹法未观察到缺血后CA1区域中GLAST和GLT-1表达的变化。EAAC1表达增强可能是对缺血期间细胞外谷氨酸水平升高的一种适应性反应。
