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Publication Detail
Arachidonic acid induces a prolonged inhibition of glutamate uptake into glial cells.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Barbour B, Szatkowski M, Ingledew N, Attwell D
  • Publication date:
    21/12/1989
  • Pagination:
    918, 920
  • Journal:
    Nature
  • Volume:
    342
  • Issue:
    6252
  • Status:
    Published
  • Country:
    England
  • Print ISSN:
    0028-0836
  • Language:
    eng
  • Keywords:
    Animals, Arachidonic Acid, Arachidonic Acids, Biological Transport, Evoked Potentials, Glutamates, In Vitro Techniques, Indomethacin, Kinetics, Masoprocol, Neuroglia, Oleic Acid, Oleic Acids, Ouabain, Retina, Tetradecanoylphorbol Acetate, Urodela
Abstract
Activation of NMDA (N-methyl-D-aspartate) receptors by neurotransmitter glutamate stimulates phospholipase A2 to release arachidonic acid. This second messenger facilitates long-term potentiation of glutamatergic synapses in the hippocampus, possibly by blocking glutamate uptake. We have studied the effect of arachidonic acid on glutamate uptake into glial cells using the whole-cell patch-clamp technique to monitor the uptake electrically. Micromolar levels of arachidonic acid inhibit glutamate uptake, mainly by reducing the maximum uptake rate with only small effects on the affinity for external glutamate and sodium. On removal of arachidonic acid a rapid (5 minutes) phase of partial recovery is followed by a maintained suppression of uptake lasting at least 20 minutes. Surprisingly, the action of arachidonic acid is unaffected by cyclo-oxygenase or lipoxygenase inhibitors suggesting that it inhibits uptake directly, possibly by increasing membrane fluidity. As blockade of phospholipase A2 prevents the induction of long-term potentiation (LTP), inhibition of glutamate uptake by arachidonic acid may contribute to the increase of synaptic gain that occurs in LTP. During anoxia, release of arachidonic acid could severely compromise glutamate uptake and thus contribute to neuronal death.
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