An endogenous cannabinoid (2-AG) is neuroprotective after brain injury.
Title | An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. |
Publication Type | Journal Article |
Year of Publication | 2001 |
Authors | Panikashvili, D., Simeonidou C., Ben-Shabat S., Hanus L., Breuer A., Mechoulam R., & Shohami E. |
Journal | Nature |
Volume | 413 |
Issue | 6855 |
Pagination | 527-31 |
Date Published | 2001 Oct 04 |
ISSN | 0028-0836 |
Keywords | Animals, 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 |
Abstract | 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. |
DOI | 10.1038/35097089 |
Alternate Journal | Nature |
PubMed ID | 11586361 |