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An endogenous cannabinoid (2-AG) is neuroprotective after brain injury.

TitleAn endogenous cannabinoid (2-AG) is neuroprotective after brain injury.
Publication TypeJournal Article
Year of Publication2001
AuthorsPanikashvili, D., Simeonidou C., Ben-Shabat S., Hanus L., Breuer A., Mechoulam R., & Shohami E.
Date Published2001 Oct 04
KeywordsAnimals, Arachidonic Acids, Body Temperature, Brain Edema, Brain Infarction, Brain Injuries, Cannabinoids, Cell Death, Disease Models, Animal, Endocannabinoids, Gas Chromatography-Mass Spectrometry, Glycerides, Head Injuries, Closed, Hippocampus, Male, Mice, Neuroprotective Agents, Receptors, Cannabinoid, Receptors, Drug

Traumatic brain injury triggers the accumulation of harmful mediators that may lead to secondary damage. Protective mechanisms to attenuate damage are also set in motion. 2-Arachidonoyl glycerol (2-AG) is an endogenous cannabinoid, identified both in the periphery and in the brain, but its physiological roles have been only partially clarified. Here we show that, after injury to the mouse brain, 2-AG may have a neuroprotective role in which the cannabinoid system is involved. After closed head injury (CHI) in mice, the level of endogenous 2-AG was significantly elevated. We administered synthetic 2-AG to mice after CHI and found significant reduction of brain oedema, better clinical recovery, reduced infarct volume and reduced hippocampal cell death compared with controls. When 2-AG was administered together with additional inactive 2-acyl-glycerols that are normally present in the brain, functional recovery was significantly enhanced. The beneficial effect of 2-AG was dose-dependently attenuated by SR-141761A, an antagonist of the CB1 cannabinoid receptor.

Alternate JournalNature
PubMed ID11586361


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