Endocannabinoid overload

Mol Pharmacol. 2010 Dec;78(6):993-5. doi: 10.1124/mol.110.069427. Epub 2010 Oct 15.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review
  • Comment

MeSH terms

  • Animals
  • Arachidonic Acids / physiology
  • Cannabinoid Receptor Modulators / physiology*
  • Down-Regulation / physiology
  • Endocannabinoids*
  • Glycerides / physiology
  • Humans
  • Monoacylglycerol Lipases / physiology
  • Receptors, Cannabinoid / physiology
  • Signal Transduction / physiology*

Substances

  • Arachidonic Acids
  • Cannabinoid Receptor Modulators
  • Endocannabinoids
  • Glycerides
  • Receptors, Cannabinoid
  • glyceryl 2-arachidonate
  • Monoacylglycerol Lipases