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Arachidonic Acid Increases Inositol Phospholipid Metabolism and Glutamate Release in Synaptosomes Prepared from Hippocampal Tissue
Author(s) -
Lynch M. A.,
Voss K. L.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb08841.x
Subject(s) - inositol , hippocampal formation , phospholipid , arachidonic acid , metabolism , glutamate receptor , chemistry , synaptosome , biochemistry , lipid metabolism , endocrinology , biology , membrane , enzyme , receptor
We have been interested in the possibility that arachidonic acid or one of its 12‐lipoxygenase metabolites may function as a retrograde messenger in long‐term potentiation (LTP) in the dentate gyrus of the hippocampus. One criterion required of a retrograde messenger is that it stimulates presynaptic changes. Here, two possible presynaptic actions of arachidonic acid and its 12‐lipoxygenase metabolites, 12‐hydroxyeicosatetraenoic acid (HETE) and 12‐hydroperoxyeicosatetraenoic acid (HPETE), are examined. We report that arachidonic acid, HETE, and HPETE significantly increase both K + ‐stimulated release of [ 3 H]glutamate and [ 3 H]inositol labelling of inositol phosphates in synaptosomes, whereas other biologically important fatty acids (oleic, palmitic, and stearic) failed to induce a similar response. The findings of these experiments are consistent with the hypothesis that arachidonic acid, HETE, or HPETE may play the role of a retrograde messenger in LTP.