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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >High expression of GLT-1 in hippocampal CA3 and dentate gyrus subfields contributes to their inherent resistance to ischemia in rats
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High expression of GLT-1 in hippocampal CA3 and dentate gyrus subfields contributes to their inherent resistance to ischemia in rats

机译：GLT-1在海马CA3和齿状回亚域中的高表达有助于其对大鼠缺血的固有抵抗力

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摘要

It is well known that neurons in the CA3 and dentate gyrus (DG) subfields of the hippocampus are resistant to short period of ischemia which is usually lethal to pyramidal neurons in hippocampal CA1 subfield. The present study was undertaken to clarify whether the inherent higher resistance of neurons in CA3 and DG to ischemia is associated with glial glutamate transporter-1 (GLT-1) in rats. Western blot analysis and immunohistochemistry assay showed that the basal expressions of GLT-1 in both CA3 and DG were much higher than that in CA1 subfield. Mild global brain ischemia for 8 min induced delayed death of almost all CA1 pyramidal neurons and marked GLT-1 down-regulation in the CA1 subfield, but it was not lethal to the neurons in either CA3 or DG and induced GLT-1 up-regulation and astrocyte activation showed normal soma and aplenty slender processes in the both areas. When the global brain ischemia was prolonged to 25 min, neuronal death was clearly observed in CA3 and DG accompanied with down-regulation of GLT-1 expression and abnormal astrocytes represented with hypertrophic somas, but shortened processes. After down-regulating of GLT-1 expression and function by its antisense oligodeoxynucleotides or inhibiting GLT-1 function by dihydrokainate, an inhibitor of GLT-1, the mild global brain ischemia for 8 min, which usually was not lethal to CA3 and DG neurons, induced the neuronal death in CA3 and DG subfields. Taken together, the higher expression of GLT-1 in the CA3 and DG contributes to their inherent resistance to ischemia.
机译：众所周知，海马CA3和齿状回（DG）子域中的神经元对短期缺血具有抵抗力，这通常对海马CA1子域的锥体神经元具有致命性。进行本研究以阐明CA3和DG中神经元固有的较高的抵抗缺血性是否与大鼠胶质谷氨酸转运蛋白-1（GLT-1）有关。 Western blot分析和免疫组化分析表明，CA3和DG中GLT-1的基础表达均明显高于CA1亚域。轻度的全球脑缺血8分钟可导致几乎所有CA1锥体神经元延迟死亡，并在CA1子域中引起GLT-1下调，但对CA3或DG中的神经元无致死作用，并导致GLT-1上调星形胶质细胞的激活在两个区域都显示出正常的体细胞和大量的细长过程。当全球脑缺血延长至25分钟时，在CA3和DG中清楚地观察到神经元死亡，并伴有GLT-1表达的下调和以肥厚性躯体为代表的异常星形胶质细胞，但过程缩短了。通过其反义寡聚脱氧核苷酸下调GLT-1的表达和功能或通过GLT-1的抑制剂dihydrokainate抑制GLT-1的功能后，轻度的全脑缺血持续8分钟，通常对CA3和DG神经元没有致死性。诱导了CA3和DG子域的神经元死亡。两者合计，CA3和DG中GLT-1的较高表达有助于其固有的抗缺血性。

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