The endocannabinoid system, one of several lipid signaling systems in the brain, is comprised of two G-protein coupled receptors, their signaling pathways, two predominant endogenous ligands, and synthetic and metabolic pathways for these endocannabinoids. Of the two identified receptors, one type (CB1) is found in largest concentrations in the brain (Herkenham et al., 1991) whereas the other type (CB2) is primarily, but not exclusively (Van Sickle et al., 2005; Xi et al., 2011), located in the periphery (Galiegue et al., 1995). Anandamide, the most thoroughly characterized of the endocannabinoids, is produced via the hydrolysis of membrane phospholipid precursors of the N-acyl-phophatidyl-ethanolamine (NAPE) family through a synthesis mechanism that has not been entirely characterized (Leung et al., 2006). Inactivation of anandamide occurs primarily via degradation by fatty acid amide hydrolase (FAAH), an enzyme that also degrades a number of other endogenous fatty acids (Cravatt and Lichtman, 2002). The primary synthetic and metabolic enzymes for the endocannabinoid 2-arachidonoylglycerol (2-AG) have been identified as diacylglycerol (DAGL) and monoacylglycerol lipase (MAGL), respectively (Dinh et al., 2002), albeit other enzymes (e.g., ABHD6 and ABHD12) also
