Majewska M D, Sun G Y
Sinclair Comparative Medicine Research Farm and Biochemistry Department, University of Missouri, Columbia, MO 65201, U.S.A.
Neurochem Int. 1982;4(5):427-33. doi: 10.1016/0197-0186(82)90086-9.
The turnover of arachidonoyl groups in synaptosomal phospholipids after stimulation by K(+) was examined. Raising the K(+) concentration in the incubation medium from 5 to 55 mM caused a rapid hydrolysis of labeled arachidonate from the synaptosomal phospholipids. Under this condition, radioactivity released from phosphatidylinositols was proportionally higher than that from phosphatidylcholines. Hydrolysis of arachidonoyl group from phospholipids was correlated to an increase in radioactivity in the free fatty acid-ion complex which appeared in the interphase after extraction with chloroform-methanol 2:1 (v/v). The K(+)-evoked phospholipid hydrolysis and the formation of fatty acid-ion complex, were Ca(2+)-dependent. Phospholipid deacylation activity was localized mainly in synaptic vesicles and synaptic plasma membranes but not in the mitochondria. The stimulated turnover of synaptosomal phospholipids appeared to be mediated by the deacylation-reacylation mechanism, because similar treatment with high K(+) stimulated the incorporation of labeled arachidonate into phosphatidylinositols and phosphatidylcholines of synaptosomes. The possible physiological implication of membrane lipid involvement in synaptic processes is discussed.
研究了钾离子（K(+)）刺激后突触体磷脂中花生四烯酰基的周转情况。将孵育培养基中的K(+)浓度从5 mM提高到55 mM会导致突触体磷脂中标记的花生四烯酸迅速水解。在此条件下，从磷脂酰肌醇释放的放射性比从磷脂酰胆碱释放的放射性成比例地更高。磷脂中花生四烯酰基的水解与在用2:1（v/v）氯仿 - 甲醇萃取后出现在界面处的游离脂肪酸 - 离子复合物中的放射性增加相关。K(+)诱发的磷脂水解和脂肪酸 - 离子复合物的形成是钙离子（Ca(2+)）依赖性的。磷脂脱酰基活性主要定位于突触小泡和突触质膜，而不是线粒体。突触体磷脂的刺激周转似乎是由脱酰基 - 再酰基化机制介导的，因为用高K(+)进行类似处理会刺激标记的花生四烯酸掺入突触体的磷脂酰肌醇和磷脂酰胆碱中。讨论了膜脂参与突触过程可能的生理意义。
