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Publication Detail
Glutamate uptake in mammalian retinal glia is voltage- and potassium-dependent.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Sarantis M, Attwell D
  • Publication date:
    21/05/1990
  • Pagination:
    322, 325
  • Journal:
    Brain Res
  • Volume:
    516
  • Issue:
    2
  • Status:
    Published
  • Country:
    Netherlands
  • Print ISSN:
    0006-8993
  • PII:
    0006-8993(90)90935-5
  • Language:
    eng
  • Keywords:
    Animals, Aspartic Acid, Carrier Proteins, Glutamates, Glutamic Acid, In Vitro Techniques, Membrane Potentials, N-Methylaspartate, Neuroglia, Neurotransmitter Agents, Potassium, Rabbits, Retina
Abstract
Glutamate evokes an inward membrane current in glial cells from the rabbit retina, by activating high-affinity glutamate uptake. Uptake is strongly inhibited by depolarization. It is also inhibited by removing extracellular sodium or intracellular potassium and by raising the extracellular potassium concentration, suggesting that the uptake carrier transports sodium ions into and potassium ions out of the cell. The voltage- and potassium-dependence of glutamate uptake may have clinical implications: during anoxia, when [K+]0 rises, uptake will be inhibited and the extracellular glutamate concentration may then rise to neurotoxic levels.
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