Trafficking of glucose, lactate, and amyloid-beta from the inferior colliculus through perivascular routes.
Trafficking of glucose, lactate, and amyloid-beta from the inferior colliculus through perivascular routes.
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DOI：
10.1038/jcbfm.2009.206
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发表时间：
2010-01
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--
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代谢脑成像被广泛用于评估脑功能和疾病，定量分析需要局部保留用于记录细胞活性变化的化合物。由于[1-和6- 14 C]葡萄糖的标记代谢物在脑激活期间快速大量释放，因此本研究评价了代谢物和蛋白质通过血管周围液体流动的释放，这是一种将溶质从脑运送到外周淋巴引流部位的途径。用[3，4 - 14 C]葡萄糖进行的测定排除了葡萄糖衍生的乳酸的局部氧化作为标记损失的主要贡献者。在声刺激期间，将[1- 14 C]葡萄糖和D-[14 C]乳酸盐短暂输注到清醒大鼠的下丘中，标记了脑膜，这与间质液中[14 C]代谢物的血管周围清除一致。微量输注伊文思蓝白蛋白和淀粉样蛋白β 1 -40引起下丘血管周围标记，标记周围脑膜，淀粉样蛋白β标记尾状核和嗅球中的特定血管，并沉积在颈部淋巴结中。细胞外葡萄糖、乳酸盐和淀粉样蛋白β流出到血管周围液体通路中是从下丘清除物质的正常途径，这有助于低估脑能量学。汇聚的“分水岭”排水共同途径可能会促进血管周围淀粉样斑块的形成和途径阻塞阿尔茨海默病。
Metabolic brain imaging is widely used to evaluate brain function and disease, and quantitative assays require local retention of compounds used to register changes in cellular activity. Because labeled metabolites of [1- and 6-14C]glucose are rapidly released in large quantities during brain activation, the present study evaluated release of metabolites and proteins via perivascular fluid flow, a pathway that carries solutes from brain to peripheral lymphatic drainage sites. Assays with [3,4-14C]glucose ruled out local oxidation of glucose-derived lactate as a major contributor of label loss. Brief infusion of [1-14C]glucose and D-[14C]lactate into the inferior colliculus of conscious rats during acoustic stimulation labeled the meninges, consistent with perivascular clearance of [14C]metabolites from interstitial fluid. Microinfusion of Evans blue albumin and amyloid-beta1–40 caused perivascular labeling in the inferior colliculus, labeled the surrounding meninges, and amyloid-beta labeled specific blood vessels in the caudate and olfactory bulb and was deposited in cervical lymph nodes. Efflux of extracellular glucose, lactate, and amyloid-beta into perivascular fluid pathways is a normal route for clearance of material from the inferior colliculus that contributes to underestimates of brain energetics. Convergence of ‘watershed’ drainage to common pathways may facilitate perivascular amyloid plaque formation and pathway obstruction in Alzheimer’s disease.
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