The study was recently published online in the journal Neuropsychopharmacology.
Notably, the research team unravelled a link between alcohol and how it modulated the levels of activity of this particular gene.
Researchers discovered that when they increased the levels of the gene encoded protein in mice, they reduced alcohol consumption by almost 50 per cent without affecting the total amount of fluid consumed or their overall well-being.
The study modified the levels of the protein encoded by a single gene - GPR39 - which is a zinc-binding receptor previously associated with depression.
Using a commercially available substance that mimics the activity of the GPR39 protein, the researchers found that targeting this gene dramatically reduced alcohol consumption in mice.
The study highlights the importance of using cross-species approaches to identify and test relevant drugs for the treatment of alcohol use disorder, said senior author Rita Cervera-Juanes.
To determine whether the same mechanism affects people, this team of researchers is now examining postmortem tissue samples from the brains of people who suffered from alcoholism.
Currently, there are only a handful of treatments for alcoholism approved by the Food and Drug Administration. By testing the effect of the substance in reducing ethanol consumption in mice - in addition to its previously reported link in reducing depression-like symptoms - the findings may point the way toward developing a drug that both prevents and treats chronic alcoholism and mood disorders in people.