Endocannabinoids accumulate in spinal cord of SOD1G93A transgenic mice

Anke Witting*, Patrick Weydt, Soyon Hong, Michel Kliot, Thomas Moller, Nephi Stella

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

78 Scopus citations

Abstract

Approximately 2% of amyotrophic lateral sclerosis (ALS) cases are caused by mutations in the super oxide dismutase 1 (SOD1) gene and transgenic mice for these mutations recapitulate many features of this devastating neurodegenerative disease. Here we show that the amount of anandamide (AEA) and 2-arachidonoylglycerol (2-AG), two endocannabinoids that have neuroprotective properties, increase in spinal cord of SOD1G93A transgenic mice. This increase occurs in the lumbar section of spinal cords, the first section to undergo neurodegeneration, and is significant before overt motor impairment. Our results show that chronic neurodegeneration induced by a genetic mutation increases endocannabinoid production possibly as part of an endogenous defense mechanism.

Original languageEnglish (US)
Pages (from-to)1555-1557
Number of pages3
JournalJournal of neurochemistry
Volume89
Issue number6
DOIs
StatePublished - Jun 2004

Keywords

  • ALS
  • Cannabinoid
  • Endocannabinoid
  • Lipids
  • SOD1

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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