Caen, France: 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 investigators from the INSERM medical research center in Caen, France and Complutense University in Madrid, 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 the likelihood of 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.”
Separate pre-clinical studies have previously documented that the administration of the non-psychotropic organic cannabinoid cannabidiol (CBD) in laboratory 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 memory, in human subjects with a history of both alcohol and marijuana use.
For more information, please contact Paul Armentano, NORML Deputy Director, at: firstname.lastname@example.org. Full text of the study, “Pharmacological Activation/Inhibition of the Cannabinoid System Affects Alcohol Withdrawal-Induced Neuronal Hypersensitivity to Excitotoxic Insults,” appears online in the journal PLoS ONE.