Trevisiol Andrea, Saab Aiman S, Winkler Ulrike, Marx Grit, Imamura Hiromi, Möbius Wiebke, Kusch Kathrin, Nave Klaus-Armin, Hirrlinger Johannes
Department of Neurogenetics, Max-Planck-Institute for Experimental Medicine, Göttingen, Germany.
Institute of Pharmacology & Toxicology, University of Zurich, Zurich, Switzerland.
Elife. 2017 Apr 17;6:e24241. doi: 10.7554/eLife.24241.
In several neurodegenerative diseases and myelin disorders, the degeneration profiles of myelinated axons are compatible with underlying energy deficits. However, it is presently impossible to measure selectively axonal ATP levels in the electrically active nervous system. We combined transgenic expression of an ATP-sensor in neurons of mice with confocal FRET imaging and electrophysiological recordings of acutely isolated optic nerves. This allowed us to monitor dynamic changes and activity-dependent axonal ATP homeostasis at the cellular level and in real time. We find that changes in ATP levels correlate well with compound action potentials. However, this correlation is disrupted when metabolism of lactate is inhibited, suggesting that axonal glycolysis products are not sufficient to maintain mitochondrial energy metabolism of electrically active axons. The combined monitoring of cellular ATP and electrical activity is a novel tool to study neuronal and glial energy metabolism in normal physiology and in models of neurodegenerative disorders.
在几种神经退行性疾病和髓鞘疾病中,有髓轴突的退化情况与潜在的能量不足相符。然而,目前在电活动的神经系统中无法选择性地测量轴突的三磷酸腺苷(ATP)水平。我们将ATP传感器在小鼠神经元中的转基因表达与共聚焦荧光共振能量转移(FRET)成像以及急性分离视神经的电生理记录相结合。这使我们能够在细胞水平实时监测动态变化和活动依赖的轴突ATP稳态。我们发现ATP水平的变化与复合动作电位密切相关。然而,当乳酸代谢受到抑制时,这种相关性就会被破坏,这表明轴突糖酵解产物不足以维持电活动轴突的线粒体能量代谢。细胞ATP和电活动的联合监测是研究正常生理学和神经退行性疾病模型中神经元和神经胶质能量代谢的一种新工具。