Asakura T, Matsuda M
Biochim Biophys Acta. 1984 Jun 27;773(2):301-7. doi: 10.1016/0005-2736(84)90094-4.
When synaptosomes were depolarized in the presence of Ca2+, or when Ca2+ was added to synaptosomes pretreated with Ca2+ ionophore (A23187), free arachidonic acid was clearly increased within synaptosomes, and at the same time an efflux of gamma-aminobutyric acid from synaptosomes was observed. Moreover, when synaptosomes labelled with [14C]arachidonic acid were depolarized in the presence of Ca2+, there was a significant decrease in the radioactivity of the fatty acid of phosphatidylinositol and phosphatidylcholine. Exogenously added arachidonic acid, but not other fatty acids, stimulated the efflux of gamma-aminobutyric acid in the absence of Ca2+. These observations suggest that the release of arachidonic acid from phospholipids is an intrinsic part of the biochemical mechanism that modulates the gamma-aminobutyric acid efflux.
当突触体在钙离子存在的情况下发生去极化时，或者当向用钙离子载体（A23187）预处理过的突触体中添加钙离子时，突触体内游离花生四烯酸明显增加，同时观察到γ-氨基丁酸从突触体中流出。此外，当用[14C]花生四烯酸标记的突触体在钙离子存在的情况下发生去极化时，磷脂酰肌醇和磷脂酰胆碱的脂肪酸放射性显著降低。在没有钙离子的情况下，外源性添加的花生四烯酸而非其他脂肪酸刺激了γ-氨基丁酸的流出。这些观察结果表明，花生四烯酸从磷脂中的释放是调节γ-氨基丁酸流出的生化机制的一个内在部分。
