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O. Payet, L. Maurin, C. Bonne, A. Muller; Hypoxia enhances glutamate uptake rate in rat retinal cells . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3272.
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Purpose: : Glutamate uptake in neurons and glial cells is essential to prevent the persistence of excitotoxic levels of glutamate observed during ischemia. The aim of the study was to investigate the effect of an acute hypoxia in vitro on glutamate transport rate in the retina. Methods: Adult rat retinal cells in suspension in Krebs/bicarbonate buffer were incubated for 3h at 37°C in humidified N2/CO2 (95/5) atmosphere ("hypoxia"). In some experiments, reoxygenation was obtained by replacing cells in air/CO2 incubator. Uptake was assessed by incubating cell suspensions for 15 min at 37°C with [3H] glutamate in isotopic dilution in the presence or absence of tested drugs. Results: A short period of hypoxia stimulated the apparent glutamate transport rate in isolated rat retinal cells. The observed increase in glutamate uptake was not affected by glutamate receptor antagonists, protein kinase inhibitors, antioxidant or neo–synthesis inhibitors. However, inhibition of actin polymerization reversed the hypoxia–induced increase in glutamate uptake, suggesting a mobilization of transporters to cell membrane. Moreover, the depletion in cell glutathione stimulated in the same manner the glutamate uptake and emphasize the key role of glutamate in the control of the level of this antioxidant. Conclusions: These results suggested that hypoxia stimulated glutamate transport traffiking to the cell membrane. This rapid up–regulation of glutamate transport could be considered as an adaptative mechanism of neuroprotection.
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