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Augmentation of Normal and Glutamate-Impaired Neuronal Respiratory Capacity by Exogenous Alternative Biofuels

机译：外源性替代生物燃料增强正常和谷氨酸受损的神经元呼吸能力

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Mitochondrial respiratory capacity is critical for responding to changes in neuronal energy demand. One approach toward neuroprotection is administration of alternative energy substrates (“biofuels”) to overcome brain injury-induced inhibition of glucose-based aerobic energy metabolism. This study tested the hypothesis that exogenous pyruvate, lactate, β-hydroxybutyrate, and acetyl-L-carnitine each increase neuronal respiratory capacity in vitro either in the absence of, or following transient excitotoxic glutamate receptor stimulation. Compared to the presence of 5 mM glucose alone, the addition of pyruvate, lactate, or β-hydroxybutyrate (1.0 – 10.0 mM) to either day in vitro (DIV) 14 or 7 rat cortical neurons resulted in significant, dose-dependent stimulation of respiratory capacity, measured by cell respirometry as the maximal O2 consumption rate in the presence of the respiratory uncoupler FCCP. A thirty minute exposure to 100 μM glutamate impaired respiratory capacity for DIV 14 but not DIV 7 neurons. Glutamate reduced the respiratory capacity for DIV 14 neurons with glucose alone by 25% and also reduced respiratory capacity with glucose plus pyruvate, lactate or β-hydroxybutyrate. However, respiratory capacity in glutamate-exposed neurons following pyruvate or β-hydroxybutyrate addition was still at least as high as that obtained with glucose alone in the absence of glutamate exposure. These results support the interpretation that previously observed neuroprotection by exogenous pyruvate, lactate, or β-hydroxybutyrate is at least partially mediated by their preservation of neuronal respiratory capacity.
机译：线粒体呼吸能力对于响应神经元能量需求的变化至关重要。一种神经保护方法是施用替代性能量底物（“生物燃料”），以克服脑损伤引起的对基于葡萄糖的有氧能量代谢的抑制。这项研究检验了以下假设：外源丙酮酸，乳酸盐，β-羟基丁酸和乙酰基L-肉碱在无或经短暂性兴奋性谷氨酸受体刺激后均能在体外增加神经元呼吸能力。与仅存在5 mM葡萄糖的情况相比，在体外（DIV）14或7个大鼠皮质神经元中添加丙酮酸，乳酸盐或β-羟基丁酸酯（1.0 – 10.0 mM）会产生显着的剂量依赖性刺激呼吸能力，通过细胞呼吸测定法在存在呼吸解偶联剂FCCP的情况下作为最大氧气消耗率来测量。暴露于100μM谷氨酸盐中30分钟会损害DIV 14而非DIV 7神经元的呼吸能力。谷氨酸盐单独使用葡萄糖可使DIV 14神经元的呼吸能力降低25％，并且在葡萄糖加丙酮酸，乳酸或β-羟基丁酸酯的作用下，谷氨酸的呼吸能力也降低。然而，添加丙酮酸或β-羟基丁酸酯后，暴露于谷氨酸的神经元的呼吸能力仍然至少与不暴露谷氨酸时单独使用葡萄糖所获得的呼吸能力一样高。这些结果支持以下解释：先前观察到的外源性丙酮酸，乳酸盐或β-羟基丁酸酯的神经保护作用至少部分是由它们对神经元呼吸能力的保存介导的。

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