• Kei Hamazaki and Hee-Yong Kim.
• Laboratory of Molecular Signaling, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health,5625 Fishers Lane, Room 3N-07, Bethesda, MD 20892-9410, United States.
• Prostaglandins Leukot. Essent. Fatty Acids. 2013 Apr 1; 88 (4): 299-306.

AbstractThe hippocampal CA1 region is most susceptible to cerebral ischemia in both rodents and humans, whereas CA3 is remarkably resistant. Here, we investigated the possible role of membrane lipids in differential susceptibility in these regions. Transient ischemia was induced in rats via bilateral occlusion of common carotid arteries and membrane lipids were analyzed by mass spectrometry. While lipid profile differences between the intact CA1 and CA3 were rather minor, ischemia caused significant pyramidal cell death with concomittant reduction of phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, plasmalogen and sphingomyelin only in CA1. The phospholipid loss was evenly distributed in most molecular species. Ischemia also significantly increased cell death mediator ceramides only in CA1. Our data suggests that differential susceptibility to ischemia between CA1 and CA3 is not linked to their unique phospholipid profile. Also, selective activation of phospholipase A2, which primarily releases polyunsaturated fatty acids, might not be characteristic to cell death in CA1.Published by Elsevier Ltd.

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