Increased Na(+)-dependent high affinity uptake of glutamate in astrocytes chronically exposed to ethanol

The effects of ethanol exposure on the Na(+)-dependent high affinity uptake of [3H]glutamate were determined in primary cultures of astrocytes prepared from neonatal rat cerebral cortex. Acute exposure to 100 mM ethanol had only marginal effects on [3H]glutamate uptake. However, chronic exposure of astrocytes to 50 or 100 mM ethanol for 4 days elicited a dose-dependent increase in the maximal uptake capacity, Vmax, for glutamate with no significant effect on the Km for this process. Because Na(+)-dependent glutamate uptake by astrocytes is considered a principal mechanism for the clearance of brain extracellular glutamate, the present results suggest that the ethanol-induced upregulation of glutamate transport may modulate glutamatergic transmission in certain disease states such as alcoholism.