Modulators of endocannabinoid enzymic hydrolysis and membrane transport.
Tissue concentrations of the endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG) are regulated by both synthesis and inactivation. The purpose of this review is to compile available data regarding three inactivation processes: fatty acid amide hydrolase, monoacylglycerol lipase, and cellular membrane transport. In particular, we have focused on mechanisms by which these processes are modulated. We describe the in vitro and in vivo effects of inhibitors of these processes as well as available evidence regarding their modulation by other factors.
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W S V
WS
Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Hillard
C J
CJ
D000581:Amidohydrolases / Q000037:antagonists & inhibitors / Q000502:physiology; D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D001692:Biological Transport; D063385:Cannabinoid Receptor Modulators / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism*; D063388:Endocannabinoids; D006801:Humans; D006868:Hydrolysis; D008994:Monoacylglycerol Lipases / Q000037:antagonists & inhibitors / Q000502:physiology; D053284:Polyunsaturated Alkamides; D013379:Substrate Specificity; D000099252:Fatty Acid Amide Hydrolases
D000581:Amidohydrolases; D001095:Arachidonic Acids; D063385:Cannabinoid Receptor Modulators; D063388:Endocannabinoids; D008994:Monoacylglycerol Lipases; D053284:Polyunsaturated Alkamides; D000099252:Fatty Acid Amide Hydrolases; C078814:anandamide