Up-regulation of neuronal and astrocytic GLT-1 mRNA in the hippocampal CA1 subfield during the induction of brain ischemic tolerance in rats.
Up-regulation of neuronal and astrocytic GLT-1 mRNA in the hippocampal CA1 subfield during the induction of brain ischemic tolerance in rats.
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DOI：
10.4449/aib.v151i2.1482
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发表时间：
2013-06
影响因子：
1
通讯作者：
Min Cao;Min Zhang-;Lianwei Zhang;Jianxue Gong;Cui-Juan Liang;Wen-Bin Li
中科院分区：
文献类型：
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作者：
Min Cao;Min Zhang-;Lianwei Zhang;Jianxue Gong;Cui-Juan Liang;Wen-Bin Li
我们之前的研究表明，3分钟脑缺血预处理（CIP）上调胶质谷氨酸转运体-1 （GLT-1）蛋白的表达，该蛋白保护锥体神经元，使它们能够在8分钟缺血损伤中存活，这种损伤通常会导致海马CA1亚区严重的延迟性神经元死亡。本研究采用原位杂交和免疫组织化学方法观察GLT-1 mRNA在脑缺血耐受诱导过程中是否被调节，以及细胞和/或神经元是否表达GLT-1 mRNA。我们观察到GLT-1 mRNA在海马CA1亚区神经元和星形胶质细胞中表达。致死性缺血性损伤8 min后，神经元和星形胶质细胞中GLT-1 mRNA的表达均显著下调。CIP作用3 min后，神经元和星形胶质细胞中GLT-1 mRNA表达增加，锥体神经元周围星形胶质细胞突起伸长。由此可见，CIP在致死性缺血性损伤前2天激活星形胶质细胞，导致表达高水平GLT-1的延长过程数量增加，从而保护神经元并使其存活8分钟，这通常对海马CA1亚区神经元是致命的。
Our previous study showed that 3-min cerebral ischemic preconditioning (CIP) up-regulated the expression of glial glutamate transporter-1 (GLT-1) protein, which protects pyramidal neurons, allowing them to survive an 8-min ischemic insult that usually induces severe delayed neuronal death in the hippocampal CA1 subfield. In the present study, in situ hybridization and immunohistochemistry were used to observe whether GLT-1 mRNA is modulated and whether actrocytes and/or neurons express GLT-1 mRNA during the induction of brain ischemic tolerance. We observed that GLT-1 mRNA is expressed in neurons and astrocytes in the hippocampal CA1 subfield. The expression of GLT-1 mRNA was significantly down-regulated in both neurons and astrocytes after the 8-min lethal ischemic insult. CIP for 3 min increased the expression of GLT-1 mRNA in neurons and astrocytes, and induced the elongation of the astrocytic processes around pyramidal neurons. It may be concluded that CIP performed 2 days before lethal ischemic insult activated astrocytes, which resulted in an increased number of lengthened processes expressing high levels of GLT-1, which protected the neurons and allowed them to survive 8-min ischemic insult that is usually lethal to neurons in the hippocampal CA1 subfield.