PMID: 8945748Nov 1, 1996Paper

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

Neuroscience Letters
T L Smith, A Zsigo

Abstract

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.

References

Jan 1, 1990·Progress in Neurobiology·M Erecińska, I A Silver
Sep 5, 1995·European Journal of Pharmacology·Z L Rossetti, S Carboni
Jul 1, 1995·Annals of Neurology·J D RothsteinR W Kuncl
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Citations

Jan 11, 2003·Neurotoxicology·Jeffrey W AllenMichael Aschner
May 23, 2001·Progress in Neurobiology·N C Danbolt
Jun 6, 2013·International Journal of Inflammation·Tazeen J AhmedCostantino Pitzalis
Nov 18, 2004·Alcoholism, Clinical and Experimental Research·Mathias ZinkRainer Spanagel
Nov 16, 2004·Annals of the New York Academy of Sciences·P F FoleyP R Dodd
Mar 25, 2014·Alcoholism, Clinical and Experimental Research·Karen L SmithAnita J Bechtholt
Apr 5, 2018·Frontiers in Molecular Neuroscience·José J Miguel-Hidalgo
Apr 21, 2017·Frontiers in Cellular Neuroscience·Juan A OrellanaRodrigo A Quintanilla

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