作者: Jochen Schacht , Bernard W. Agranoff
DOI: 10.1016/S0021-9258(19)42918-9
关键词: Phosphatidic acid 、 Internal medicine 、 Phosphatidate 、 Chemistry 、 Inositol 、 Phosphatidylinositol 、 Cholinergic 、 Phospholipid 、 Endocrinology 、 Stimulation 、 Biochemistry 、 Acetylcholine 、 Cell biology 、 Molecular biology
摘要: Abstract "Light" nerve endings from guinea pig cerebral cortex were incubated with [32P]orthophosphate, myo[3H]inositol, [3H]glycerol, or [3H]glucose in the presence absence of cholinergic agents. Acetylcholine and carbamylcholine increased incorporation 32Pi into phosphatidic acid 100% various classes phosphatidylinositol 20 to 70%. These agents also stimulated labeling myo[3H]inositol but did not affect either [3H]glycerol [3H]glucose. The specific activity synaptosomal [γ-32P]ATP was unchanged. In a series two-step incubations, lipids first labeled 32Pi, then excess unlabeled Pi 2,4-dinitrophenol added lower amount [γ32P]-ATP. addition acetylcholine rate disappearance [32P]phosphatidic by 80%. This effect blocked atropine. We conclude that increase phospholipid increasing hydrolysis phosphatidate.