Changes in brain levels of N-acylethanolamines and 2-arachidonoylglycerol in focal cerebral ischemia in mice

Matilda Degn, Kate L Lambertsen, Gitte Petersen, Michael Meldgaard, Andreas Artmann, Bettina H Clausen, Steen H. Hansen, Bente Finsen, Harald S Hansen, Trine M Lund

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

The N-acylethanolamines (NAEs) and 2-arachidonoylglycerol (2-AG) are bioactive lipids that can modulate inflammatory responses and protect neurons against glutamatergic excitotoxicity. We have used a model of focal cerebral ischemia in young adult mice to investigate the relationship between focal cerebral ischemia and endogenous NAEs. Over the first 24 h after induction of permanent middle cerebral artery occlusion, we observed a time-dependent increase in all the investigated NAEs, except for anandamide. Moreover, we found an accumulation of 2-AG at 4 h that returned to basal level 12 h after induction of ischemia. Accumulation of NAEs did not depend on regulation of N-acylphosphatidylethanolamine-hydrolyzing phospholipase D or fatty acid amide hydrolase. Treatment with the fatty acid amide hydrolase inhibitor URB597 (cyclohexyl carbamic acid 3'-carbamoyl-biphenyl-3-yl ester; 1 mg/kg; i.p.) 1.5 h before arterial occlusion decreased the infarct volume in our model system. Our results suggest that NAEs and 2-AG may be involved in regulation of neuroprotection during focal cerebral ischemia in mice.
Original languageEnglish
JournalJournal of Neurochemistry
Volume103
Issue number5
Pages (from-to)1907-16
Number of pages9
ISSN0022-3042
DOIs
Publication statusPublished - 1. Dec 2007

Keywords

  • Analysis of Variance
  • Animals
  • Arachidonic Acids
  • Benzamides
  • Brain
  • Brain Infarction
  • Brain Ischemia
  • Carbamates
  • Disease Models, Animal
  • Enzyme Inhibitors
  • Ethanolamines
  • Glycerides
  • Male
  • Mice
  • RNA, Messenger
  • Time Factors

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