Quantitative immunocytochemistry (image analysis) of glucose transporters in the normal and postischemic rodent hippocampus.

Quantitative immunocytochemistry (image analysis) of glucose transporters in the normal and postischemic rodent hippocampus.
复制标题

正常和缺血后啮齿动物海马中葡萄糖转运蛋白的定量免疫细胞化学(图像分析)。

DOI:
10.1038/jcbfm.1991.85
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发表时间:
1991
期刊:
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
影响因子:
--
通讯作者:
Drewes,LR
Drewes,LR
中科院分区:
--
文献类型:
--
作者:
Gerhart,DZ;Djuricic,B;Drewes,LR

文献摘要

相似文献

采用双侧颈动脉闭塞模型和大鼠脑/人肝癌葡萄糖转运蛋白羧基末端多克隆抗体,定量检测沙鼠海马微血管转运蛋白在缺血6-7.5 min后的变化。对缺血后2小时、3天、6天、4周和7周死亡的沙鼠冷冻切片进行图像分析,测定CA亚区下方空隙层分子层(SLM)中免疫细胞化学染色微血管的光学密度。微血管在东方层、金字塔层和辐射状层中分布稀疏。相比之下,上皮层血管化程度相对较好,这种微血管分布在缺血后持续存在。仅根据对照沙鼠和ca1锥体细胞完全破坏的沙鼠的微血管分布就可以识别出SLM。SLM微血管中葡萄糖转运蛋白的丰度保持不变,这表明该蛋白的下调不能解释脑葡萄糖利用率下降和缺血后细胞死亡的原因。相反,锥体细胞CA的存在和代谢活性似乎不是海马微血管中葡萄糖转运蛋白丰度的决定因素。沙鼠和大鼠的脑微血管和脉络膜丛上皮细胞中含有丰富的脑/肝癌葡萄糖转运体。海马神经节的染色不强烈,定位不佳,在光镜下,与特定细胞类型没有明确的联系。
The bilateral carotid occlusion model and a polyclonal antibody to the carboxyl terminus of the rat brain/human hepatoma glucose transporter were used to examine quantitatively changes in the transporter in gerbil hippocampal microvessels following 6–7.5 min of ischemia. The optical densities of immunocytochemically stained microvessels in the stratum lacunosum-moleculare (SLM) below the CA, subfield were determined using image analysis of frozen sections from gerbils killed 2 h, 3 days, 6 days, 4 weeks, and 7 weeks after the ischemic episode. Microvessels were sparsely distributed in the stratum oriens, stratum pyramidale, and stratum radiatum. In contrast, the SLM was relatively well vascularized, and this distribution of microvessels persisted following ischemia. The SLM was identifiable based solely on microvessel distribution both in control gerbils and in gerbils that exhibited complete destruction of CA1pyramidal cells. The abundance of the glucose transporter in SLM microvessels remained constant, suggesting that down-regulation of this protein cannot account for reported declines in brain glucose utilization and cell death following ischemia. Conversely, the presence and metabolic activity of CA, pyramidal cells do not appear to be determinants of glucose transporter abundance in hippocampal microvessels. The brain/hepatoma glucose transporter was abundant in brain microvessels and the epithelial cells of the choroid plexus of gerbil and rat. Staining of hippocampal neuropil was less intense, poorly localized, and, at the light microscope level, not clearly associated with a particular cell type.