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Inositol phospholipids are probably not the source of arachidonic acid for eicosanoid synthesis in astrocytes
Author(s) -
Pearce Brian,
Jeremy Jamie,
Morrow Christine,
Murphy Sean,
Dandona Paresh
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)81277-2
Subject(s) - arachidonic acid , inositol , eicosanoid , phospholipase a2 , phospholipid , liberation , biochemistry , chemistry , astrocyte , receptor , eicosanoid metabolism , inositol trisphosphate , phospholipase c , biology , endocrinology , in vitro , central nervous system , membrane , enzyme
In astrocyte‐enriched cultures of the rat cerebral cortex the Ca 2+ ionophore A23187 provoked the breakdown of inositol phospholipids, the liberation of arachidonic acid and the release of prostaglandins E 2 , F 2α , I 2 and thromboxane A 2 . However, agonists for receptors also coupled to inositol phospholipid metabolism in these cells failed to produce an increase in the release of both arachidonic acid and eicosanoids. Results suggest that the A23187‐stimulated release of arachidonic acid and eicosanoids is caused by a phospholipase A 2 ‐mediated attack on lipids other than the inositol phospholipids. Moreover, receptors linked to inositol lipid turnover are not involved in the control of eicosanoid release from astrocytes.