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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 >Immunohistochemical and in situ hybridization studies on glycine transporter 1 after transient ischemia in the rat forebrain.
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Immunohistochemical and in situ hybridization studies on glycine transporter 1 after transient ischemia in the rat forebrain.

机译：大鼠前脑短暂性缺血后甘氨酸转运蛋白1的免疫组织化学和原位杂交研究。

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摘要

Glycine is a critical factor in ischemia as reduced astrocytic and increased extracellular glycine levels aggravate the neurotoxic effect of glutamate and consequently, increase the extent of brain damage. Extracellular levels of glycine are primarily regulated by the plasma membrane glycine transporter 1. In the present study, we examined the effects of transient ischemia (1 h occlusion of the middle cerebral artery; followed by 0 h, 0.5 h, 1 h, 2 h, 4 h, 24 h or 48 h reperfusion) on immunoreactivity and mRNA expression of glycine transporter 1 in the rat forebrain. In control animals, glycine transporter 1-immunoreactivity was strong in diencephalic and certain telencephalic structures, moderate in the globus pallidus, and rather low in the cortex and striatum. In situ hybridization studies revealed a similar distribution pattern of glycine transporter 1 mRNA expression. One hour occlusion of the middle cerebral artery resulted in a significant decrease in ipsilateral glycine transporter 1-immunoreactivity and mRNA expression in a circumscribed region of the preoptic/hypothalamic area; both the immunoreactivity and mRNA exhibited further reductions with increasing reperfusion time. In contrast, the cerebral cortex and the globus pallidus showed an increase of glycine transporter 1-immunoreactivity after 0.5 h reperfusion; the elevation proved to be transient in the somatosensory cortex and remained sustained in the globus pallidus after longer reperfusion times. Western blot analysis of globus pallidus samples from the ipsilateral side confirmed higher glycine transporter 1 protein levels. These results suggest an elevated expression of the transporter protein facilitating the glial uptake of glycine from the extracellular space. However, glycine transporter 1 mRNA expression was not significantly different in the penumbra regions from the corresponding contralateral sites of the injury. Together, these findings indicate that post-translational mechanisms are of primary importance in elevating glycine transporter 1 protein levels following transient ischemia.
机译：甘氨酸是缺血的关键因素，因为星形胶质细胞的减少和细胞外甘氨酸水平的增加会加剧谷氨酸的神经毒性作用，因此会增加脑损伤的程度。胞外甘氨酸水平主要受质膜甘氨酸转运蛋白1调节。在本研究中，我们检查了短暂性缺血（大脑中动脉闭塞1 h;随后0 h，0.5 h，1 h，2 h ，4 h，24 h或48 h再灌注）对大鼠前脑中甘氨酸转运蛋白1的免疫反应性和mRNA表达的影响。在对照动物中，甘氨酸转运蛋白1-免疫反应性在二脑和某些远脑结构中较强，在苍白球中中等，而在皮质和纹状体中较低。原位杂交研究揭示了甘氨酸转运蛋白1 mRNA表达的相似分布模式。大脑中动脉闭塞一小时导致视前/下丘脑区域的边界区域同侧甘氨酸转运蛋白1-免疫反应性和mRNA表达显着降低。随着再灌注时间的增加，免疫反应性和mRNA均表现出进一步的降低。相反，再灌注0.5h后，大脑皮层和苍白球显示出甘氨酸转运蛋白1的免疫反应增加。在较长的再灌注时间之后，这种升高在体感皮层中是短暂的，在苍白球中仍然持续。来自同侧的苍白球样品的蛋白质印迹分析证实了较高的甘氨酸转运蛋白1蛋白水平。这些结果表明转运蛋白的表达升高，促进神经胶质从细胞外空间摄取甘氨酸。但是，甘氨酸转运蛋白1 mRNA的表达在半影区与损伤的相应对侧部位没有显着差异。总之，这些发现表明，在短暂性缺血后，翻译后机制对于提高甘氨酸转运蛋白1的蛋白水平至关重要。

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