PT  - JOURNAL ARTICLE
AU  - Aron H. Lichtman
AU  - Jacqueline L. Blankman
AU  - Benjamin F. Cravatt
TI  - Endocannabinoid Overload
AID  - 10.1124/mol.110.069427
DP  - 2010 Dec 01
TA  - Molecular Pharmacology
PG  - 993--995
VI  - 78
IP  - 6
4099  - http://molpharm.aspetjournals.org/content/78/6/993.short
4100  - http://molpharm.aspetjournals.org/content/78/6/993.full
SO  - Mol Pharmacol2010 Dec 01; 78
AB  - The signaling capacity of endogenous cannabinoids (“endocannabinoids”) is tightly regulated by degradative enzymes. This Perspective highlights a research article in this issue (p. 996) in which the authors show that genetic disruption of monoacylglycerol lipase (MAGL), the principal degradative enzyme for the endocannabinoid 2-arachidonoylglycerol (2-AG), causes marked elevations in 2-AG levels that lead to desensitization of brain cannabinoid receptors. These findings highlight the central role that MAGL plays in endocannabinoid metabolism in vivo and reveal that excessive 2-AG signaling can lead to functional antagonism of the brain cannabinoid system.