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.
Smith
T L
TL
Department of Veterans Affairs Medical Center, Tucson, Arizona 85723, USA.
Zsigo
A
A
D000818:Animals; D001253:Astrocytes / Q000187:drug effects*; D000431:Ethanol / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000494:pharmacology*; D013997:Time Factors
D000431:Ethanol; D018698:Glutamic Acid; D012964:Sodium