關(guān)鍵詞：非損傷微測技術(shù)(a self-referencing O2 electrode), 氧氣消耗量(oxygen consumption), 谷氨酸(glutamate);
參考文獻(xiàn)：Gleichmann M, et al. J Neurochem, 2009,109: 644-655
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Abstract：
In order to determine the sequence of cellular processes in glutamate toxicity, we simultaneously recorded O2 consumption,cytosolic Ca2+ concentration ([Ca2+]i), and mitochondrial membrane potential (mDw) in single cortical neurons. Oxygen consumption was measured using an amperometric selfreferencing platinum electrode adjacent to neurons in which [Ca2+]i and mDw were monitored with Fluo-4 and TMRE+,respectively, using a spinning disk laser confocal microscope.Excitotoxic doses of glutamate caused an elevation of [Ca2+]i followed seconds afterwards by an increase in O2 consumption which reached a maximum level within 1–5 min. A modest increase in mDw occurred during this time period, and then, shortly before maximalO2 consumption was reached, themDw, as indicated by TMRE+ fluorescence, dissipated. Maximal O2 consumption lasted up to 5 min and then declined together with mDw and ATP levels, while [Ca2+]i further increased. mDw and [Ca2+]i returned to baseline levels when neurons were treated
with an NMDA receptor antagonist shortly after the [Ca2+]i increased. Our unprecedented spatial and time resolution revealed that this sequence of events is identical in all neurons, albeit with considerable variability in magnitude and kinetics of changes in O2 consumption, [Ca2+]i, and mDw. The data obtained using this new method are consistent with a model where Ca2+ influx causes ATP depletion, despite maximal mitochondrial respiration, minutes after glutamate receptor activation.
Keywords: excitotoxicity, glutamate, oxygen consumption.