Fig. 5. After 90 min of oxygen–glucose deprivation (OGD), the protective effect of sevoflurane on glutamate uptake seemed to be mediated by the glial glutamate transporter (GLT1). Uptake experiments were performed at the end of the injury, before reoxygenation. Experiments were performed in the presence or absence of 300 μm threo-3-methyl glutamate (3MG), a rather selective inhibitor of GLT1. 3MG decreased the glutamate uptake rate but did not further affect this activity after 90 min of OGD. Moreover, the glutamate uptake rate measured in OGD cells treated with 3.4 mm sevoflurane decreased significantly in the presence of 3MG. n = 12; *  P < 0.05  versus without 3MG. 

Fig. 5. After 90 min of oxygen–glucose deprivation (OGD), the protective effect of sevoflurane on glutamate uptake seemed to be mediated by the glial glutamate transporter (GLT1). Uptake experiments were performed at the end of the injury, before reoxygenation. Experiments were performed in the presence or absence of 300 μm threo-3-methyl glutamate (3MG), a rather selective inhibitor of GLT1. 3MG decreased the glutamate uptake rate but did not further affect this activity after 90 min of OGD. Moreover, the glutamate uptake rate measured in OGD cells treated with 3.4 mm sevoflurane decreased significantly in the presence of 3MG. n = 12; *  P < 0.05  versus without 3MG. 

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