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

Author

Listed:
  • David Panikashvili

    (Medical Faculty, Hebrew University
    Medical Faculty, Hebrew University)

  • Constantina Simeonidou

    (Medical Faculty, Hebrew University)

  • Shimon Ben-Shabat

    (Medical Faculty, Hebrew University)

  • Lumír Hanuš

    (Medical Faculty, Hebrew University)

  • Aviva Breuer

    (Medical Faculty, Hebrew University)

  • Raphael Mechoulam

    (Medical Faculty, Hebrew University)

  • Esther Shohami

    (Medical Faculty, Hebrew University)

Abstract

Traumatic brain injury triggers the accumulation of harmful mediators that may lead to secondary damage1,2. Protective mechanisms to attenuate damage are also set in motion2. 2-Arachidonoyl glycerol (2-AG) is an endogenous cannabinoid, identified both in the periphery3 and in the brain4, but its physiological roles have been only partially clarified5,6,7. 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.

Suggested Citation

  • David Panikashvili & Constantina Simeonidou & Shimon Ben-Shabat & Lumír Hanuš & Aviva Breuer & Raphael Mechoulam & Esther Shohami, 2001. "An endogenous cannabinoid (2-AG) is neuroprotective after brain injury," Nature, Nature, vol. 413(6855), pages 527-531, October.
    • Handle: RePEc:nat:nature:v:413:y:2001:i:6855:d:10.1038_35097089
    DOI: 10.1038/35097089
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    Cited by:

    1. Ana Belen Lopez-Rodriguez & Estefania Acaz-Fonseca & Maria-Paz Viveros & Luis M Garcia-Segura, 2015. "Changes in Cannabinoid Receptors, Aquaporin 4 and Vimentin Expression after Traumatic Brain Injury in Adolescent Male Mice. Association with Edema and Neurological Deficit," PLOS ONE, Public Library of Science, vol. 10(6), pages 1-17, June.

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