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Arachidonic acid release from K(+)-evoked depolarization of brain synaptosomes.

作者信息

Lazarewicz J W, Leu V, Sun G Y, Sun A Y

机构信息

Sinclair Comparative Medicine Research Farm and Department of Biochemistry, University of Missouri, Columbia, MO 65201, U.S.A.

出版信息

Neurochem Int. 1983;5(4):471-8. doi: 10.1016/0197-0186(83)90077-3.

DOI:10.1016/0197-0186(83)90077-3
PMID:20487975
Abstract

Rat brain synaptosomes prelabeled with [(14)C]arachidonate in their phospholipids were superfused with well oxygenated Krebs-Ringer-bicarbonate solution containing 0.2% BSA and subsequently depolarized by elevating the K(+) concentration in the superfusion medium from 5 to 55 mM. The efflux of labeled arachidonate at steady state was 0.19% (n = 12) of total radioactivity per min. In the presence of 2.5 mM Ca(2+), high K(+) (55 mM) in the medium elicited an increase in arachidonate efflux which amounted to 121.4% (n = 6) of control. Both Ca(2+) and BSA were required for the stimulated efflux of arachidonate during K(+)-depolarization. Under the same condition, K(+)-stimulation also evoked the release of [(3)H]norepinephrine which was preloaded into the synaptosomes prior to superfusion. EGTA abolished the stimulated release of both arachidonate and norepinephrine during K(+)-depolarization. These results, together with the loss of labeled arachidonic acid from phospholipids (Majewska and Sun, 1982), indicate that deacylation of membrane lipids is involved in synaptic functions.

摘要

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