Activation of arachidonoyl-phosphatidylinositol and phosphatidylcholine turnover by K(+)-evoked stimulation of brain synaptosomes.
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.
Majewska
M D
MD
Sinclair Comparative Medicine Research Farm and Biochemistry Department, University of Missouri, Columbia, MO 65201, U.S.A.
Sun
G Y
GY