Rat brain arachidonic acid metabolism is increased by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide
Article first published online: 27 JAN 2004
Journal of Neurochemistry
Volume 88, Issue 5, pages 1168–1178, March 2004
How to Cite
Rosenberger, T. A., Villacreses, N. E., Hovda, J. T., Bosetti, F., Weerasinghe, G., Wine, R. N., Harry, G. J. and Rapoport, S. I. (2004), Rat brain arachidonic acid metabolism is increased by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide. Journal of Neurochemistry, 88: 1168–1178. doi: 10.1046/j.1471-4159.2003.02246.x
- Issue published online: 4 FEB 2004
- Article first published online: 27 JAN 2004
- Resubmitted manuscript received September 14, 2003; accepted October 28, 2003.
- arachidonic acid;
- phospholipase A2;
In a rat model of acute neuroinflammation, produced by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide (LPS), we measured brain activities and protein levels of three phospholipases A2 (PLA2) and of cyclo-oxygenase-1 and -2, and quantified other aspects of brain phospholipid and fatty acid metabolism. The 6-day intracerebral ventricular infusion increased lectin-reactive microglia in the cerebral ventricles, pia mater, and the glial membrane of the cortex and resulted in morphological changes of glial fibrillary acidic protein (GFAP)-positive astrocytes in the cortical mantel and areas surrounding the cerebral ventricles. LPS infusion increased brain cytosolic and secretory PLA2 activities by 71% and 47%, respectively, as well as the brain concentrations of non-esterified linoleic and arachidonic acids, and of prostaglandins E2 and D2. LPS infusion also increased rates of incorporation and turnover of arachidonic acid in phosphatidylethanolamine, plasmenylethanolamine, phosphatidylcholine, and plasmenylcholine by 1.5- to 2.8-fold, without changing these rates in phosphatidylserine or phosphatidylinositol. These observations suggest that selective alterations in brain arachidonic acid metabolism involving cytosolic and secretory PLA2 contribute to early pathology in neuroinflammation.