[Editor’s note: This post is excerpted from this week’s forthcoming NORML weekly media advisory. To have NORML’s media alerts and legislative advisories delivered straight to your in-box, sign up here. To watch NORML’s weekly video summary of the week’s top stories, click here.] The administration of the synthetic cannabinoid agonist HU-211 decreases nerve cell death in an in vitro model of ethanol withdrawal, according to data published online in the journal of the Public Library of Science (PLoS ONE).
An international team of researchers from France and Spain assessed the anti-excitotoxic effects of the synthetic cannabinoid HU-211 in culture. Researchers demonstrated that cannabinoid administration protected neurons from cell death in an experimental model of ethanol withdrawal. By contrast, the administration of a cannabinoid antagonist (rimonabant) during ethanol withdrawal greatly increased cell death.
“[T]hese observations show, for the first time, that the stimulation of the endocannabinoid system could be protective against the hyper-excitability developed during alcohol withdrawal,” investigators concluded. “By contrast, the blockade of the endocannabinoid system seems to be counterproductive during alcohol withdrawal.”
In humans, the abrupt cessation of alcohol in dependent subjects may be associated with tremor, delirium, brain damage, and death.
Separate pre-clinical studies have previously documented that administration of the non-psychotropic organic cannabinoid cannabidiol (CBD) in animals is neuroprotective against cerebral infarction and ethanol-induced neurotoxicity (alcohol poisoning).
In 2009 and 2010, a pair of studies conducted by investigators at the University of California at San Diego reported that the consumption of cannabis may offset certain alcohol-induced brain abnormalities, including the loss of white matter integrity and impaired memory, in human subjects with a history of both alcohol and marijuana use.
Full text of the study appears online in PLoS ONE here.