Functional significance of the preconditioning-induced down-regulation of glutamate transporter GLT-1 in neuron/astrocyte co-cultures
Functional significance of the preconditioning-induced down-regulation of glutamate transporter GLT-1 in neuron/astrocyte co-cultures
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DOI：
10.1007/s11064-005-8219-z
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发表时间：
2005-09-01
影响因子：
4.4
通讯作者：
Tanaka, M
中科院分区：
文献类型：
--
作者：
Kosugi, T;Kawahara, K;Tanaka, M
在大脑中，已知先前的亚致死性缺血（预处理，PC）会产生神经元对随后的致死性缺血的耐受性。本研究旨在阐明 PC 治疗在神经元和/或星形胶质细胞中引起的改变。先前的PC治疗显着抑制了缺血期间细胞外谷氨酸浓度的升高。免疫细胞化学和蛋白质印迹分析表明，PC 损伤后星形胶质细胞谷氨酸转运蛋白 GLT-1 的表达短暂下调。 PC 损伤可能抑制上调 GLT-1 的神经元衍生因子。在这里，我们表明 PC 诱导的 GLT-1 下调对于增加神经元对随后严重缺血性损伤的抵抗力至关重要。
In the brain, prior sublethal ischemia (preconditioning, PC) is known to produce tolerance of neurons to subsequent lethal ischemia. This study aims at elucidating what alterations were induced in neurons and/or astrocytes by PC treatment. The rise in the extracellular concentration of glutamate during ischemia was markedly suppressed by the prior PC treatment. Immunocytochemical and Western blot analyses demonstrated that the expression of the astrocytic glutamate transporter GLT-1 was transiently down-regulated after the PC insult. The PC insult possibly suppressed the neuron-derived factors up-regulating GLT-1. Here we show that PC-induced down-regulation of GLT-1 is crucial for the increased neuronal resistance to subsequent severe ischemic insult.