J. Lipid Res.
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A more recent version of this article appeared on February 1, 2005

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J. Lipid Res., doi:10.1194/jlr.M400377-JLR200
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Submitted on September 30, 2004
Revised on November 17, 2004
Accepted on November 18, 2004

The post-mortal accumulation of brain N-arachidonylethanolamine (anandamide) is dependent upon fatty acid amide hydrolase activity

Sachin Patel, Erica J. Carrier, W.-S. Vanessa Ho, David J. Rademacher, Sonya Cunningham, D. Sudarshan Reddy, J. R. Falck, Benjamin F. Cravatt, and Cecilia J. Hillard

Pharmacology Dept., Medical College of Wisconsin, Milwaukee, WI 53226

Corresponding Author: chillard{at}mcw.edu

N-Arachidonylethanolamine (AEA) accumulates during brain injury and post-mortem. Since fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the post-mortal accumulation of AEA using FAAH null mice. As expected, AEA content in immediately frozen brain tissue was significantly greater in FAAH-/- than wild type mice. However, AEA content was significantly lower in brains from FAAH-/- mice at 5 and 24 h post-mortem. Similarly, wild type mice treated in vivo with a FAAH inhibitor (URB532) had significantly lower brain AEA content 24 h post-mortem compared to controls. These data indicate that FAAH contributes significantly to the post-mortal accumulation of AEA. In contrast, the accumulation of two other N-acylethanolamines, oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) were not reduced at 24 h post-mortem in either the FAAH-/- mice or in mice treated with URB532. FAAH-/- mice accumulated significantly less ethanolamine at 24 h post-mortem compared to wild-type mice, suggesting that FAAH activity plays a role in the accumulation of ethanolamine post-mortem. These data demonstrate that FAAH activity differentially affects AEA and OEA/PEA contents post-mortem and suggest that AEA formation specifically occurs via an ethanolamine-dependent route post-mortem.


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