Murphy S, Welk G
Department of Pharmacology, College of Medicine, University of Iowa, Iowa City 52242.
Neurosci Lett. 1990 Feb 5;109(1-2):152-6. doi: 10.1016/0304-3940(90)90554-m.
In response to ATP, astrocytes accumulate inositol phosphates and release arachidonic acid (AA) from phospholipid stores, events which may be linked through intracellular calcium mobilization and activation of phospholipase A2. When cells were exposed to ATP in the presence of serotonin there was a dose-dependent inhibition of AA release, an effect which was reversed by methysergide. However, the accumulation of inositol phosphates due to ATP was elevated in the presence of serotonin, and this effect was again reversed by methysergide. The mechanism by which serotonin inhibits ATP-induced arachidonate mobilization does not, therefore, involve the purinergic receptor or its coupling to inositol phospholipid pools. The hydrolysis of polyphosphoinositides by serotonin and subsequent generation of inositol trisphosphate may deplete a specific intracellular calcium store normally available to ATP, the mobilization of which stimulates phospholipase A2 and thus AA release.
作为对ATP的反应，星形胶质细胞积累肌醇磷酸，并从磷脂储存中释放花生四烯酸（AA），这些事件可能通过细胞内钙动员和磷脂酶A2的激活而联系起来。当细胞在血清素存在的情况下暴露于ATP时，AA释放受到剂量依赖性抑制，这种作用可被麦角新碱逆转。然而，在血清素存在的情况下，由于ATP导致的肌醇磷酸积累增加，并且这种作用再次被麦角新碱逆转。因此，血清素抑制ATP诱导的花生四烯酸动员的机制不涉及嘌呤能受体或其与肌醇磷脂池的偶联。血清素对多磷酸肌醇的水解以及随后肌醇三磷酸的生成可能会耗尽ATP通常可利用的特定细胞内钙储存，其动员刺激磷脂酶A2，从而释放AA。
