Arachidonic acid evokes inositol phospholipid hydrolysis in astrocytes.
Astrocyte cultures prelabelled with [3H]inositol were exposed to arachidonic acid (AA) in the presence and absence of various agonists. AA alone evoked a dose-dependent increase in the accumulation of inositol phosphates (IP), an effect not secondary to eicosanoid synthesis and release but which was abolished by EGTA. Separation of the IP revealed that AA stimulated increases in inositol tris-, bis- and monophosphates. IP formation evoked by carbachol or norepinephrine was additive with AA, whereas IP formation by platelet activating factor (PAF) or ATP was non-additive with AA. These results suggest that AA released upon stimulation of astrocytes or other cells in the CNS could initiate and/or amplify intercellular signalling.
Murphy
S
S
Department of Pharmacology, College of Medicine, University of Iowa, Iowa City 52242.
Welk
G
G
D000818:Animals; D000831:Animals, Newborn; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology*; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000378:metabolism; D006868:Hydrolysis; D007294:Inositol / Q000378:metabolism; D007295:Inositol Phosphates / Q000378:metabolism*; D007700:Kinetics; D009638:Norepinephrine / Q000494:pharmacology; D010972:Platelet Activating Factor / Q000494:pharmacology; D051381:Rats
D001095:Arachidonic Acids; D007295:Inositol Phosphates; D010972:Platelet Activating Factor; D016718:Arachidonic Acid; D007294:Inositol; D002217:Carbachol; D009638:Norepinephrine