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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Neuropharmacology. 2013 Aug 13:S0028-3908(13)00343-2 10.1016/j.neuropharm.2013.07.026. doi: 10.1016/j.neuropharm.2013.07.026

Figure 1. Formation and deactivation of 2-AG in brain neurons.

Figure 1

Receptor-operated phospholipase C-β (PLC-β) converts phosphatidylinositol-4,5-bisphosphate (PIP2) into 1,2-diacylglycerol (DAG). DAG is hydrolyzed by diacylglycerol lipase-α (DGL-α) forming 2-AG. 2-AG is subjected to hydrolytic cleavage catalyzed by either monoacylglycerol lipase (MGL) or α/β hydrolase domain-containing protein 6 (ABHD-6). Additionally, 2-AG can be dioxygenated by cyclooxygenase-2 (Cox-2) to yield a family of non-endocannabinoid prostaglandin (PG) glyceryl esters. Free arachidonic acid (AA) is converted into the eicosanoid family of compounds, for example prostacyclin (PGI2), by cyclooxygenase or lipoxygenase enzymes.