Glutamate Impairs Mitochondria Aerobic Respiration Capacity and Enhances Glycolysis in Cultured Rat Astrocytes |
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Authors: | YAN Xu SHI Zhong Fang XU Li Xin LI Jia Xin WU Min WANG Xiao Xuan JIA Mei DONG Li Ping YANG Shao Hua YUAN Fang |
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Affiliation: | 1. Department of Pathophysiology, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China;2. Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, Texas 76107-2699, USA |
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Abstract: | Objective To study the effect of glutamate on metabolism, shifts in glycolysis and lactate release in rat astrocytes. Methods After 10 days, secondary cultured astrocytes were treated with 1 mmol/L glutamate for 1 h, and the oxygen consumption rates (OCR) and extra cellular acidification rate (ECAR) was analyzed using a Seahorse XF 24 Extracellular Flux Analyzer. Cell viability was then evaluated by MTT assay. Moreover, changes in extracellular lactate concentration induced by glutamate were tested with a lactate detection kit. Results Compared with the control group, treatment with 1 mmol/L glutamate decreased the astrocytes’ maximal respiration and spare respiratory capacity but increased their glycolytic capacity and glycolytic reserve. Further analysis found that 1-h treatment with different concentrations of glutamate (0.1-1 mmol/L) increased lactate release from astrocytes, however the cell viability was not affected by the glutamate treatment. Conclusion The current study provided direct evidence that exogenous glutamate treatment impaired the mitochondrial respiration capacity of astrocytes and enhanced aerobic glycolysis, which could be involved in glutamate injury or protection mechanisms in response to neurological disorders. |
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Keywords: | Astrocytes Glutamate Mitochondrial metabolism Glycolysis Lactate |
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