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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.
T L Smith, and
A Zsigo
January 1997,
Life sciences,
T L Smith, and
A Zsigo
July 1999,
Neuroscience letters,
T L Smith, and
A Zsigo
April 1992,
FEBS letters,
T L Smith, and
A Zsigo
August 1993,
European journal of pharmacology,
T L Smith, and
A Zsigo
February 1976,
Life sciences,
T L Smith, and
A Zsigo
May 2000,
Journal of immunology (Baltimore, Md. : 1950),
T L Smith, and
A Zsigo
February 1997,
Glia,
T L Smith, and
A Zsigo
March 1994,
Biochemical and biophysical research communications,
T L Smith, and
A Zsigo
February 1980,
Brain research,
T L Smith, and
A Zsigo
May 1991,
Brain research,
