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Changes in brain levels of N ‐acylethanolamines and 2‐arachidonoylglycerol in focal cerebral ischemia in mice
Author(s) -
Degn Matilda,
Lambertsen Kate L,
Petersen Gitte,
Meldgaard Michael,
Artmann Andreas,
Clausen Bettina H,
Hansen Steen H,
Finsen Bente,
Hansen Harald S,
Lund Trine M
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04892.x
Subject(s) - fatty acid amide hydrolase , anandamide , neuroprotection , 2 arachidonoylglycerol , ischemia , chemistry , pharmacology , endocannabinoid system , brain ischemia , biochemistry , endocrinology , anesthesia , medicine , cannabinoid receptor , receptor , agonist
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.