Lack of a brain protein could play a role in promoting binge drinking behaviour. A drug to boost this protein could actually prevent drinking to the point of intoxication, says a study.
They found that deleting the gene for this protein in mice ramped up alcohol consumption and prevented the brain from signalling the rewarding properties of alcohol.
This has led the researchers to believe that a compound selectively targeting the protein GIRK3 -- G protein-gated inwardly rectifying potassium channel -- may hold promise for reducing alcohol consumption in heavy binge drinkers.
"Our study sheds light on the molecular mechanisms implicated in binge drinking," said senior author of the study Candice Contet from The Scripps Research Institute (TSRI) in the US.
The researchers investigated how GIRK3 influenced mouse behaviour and neuronal function in the presence of alcohol. To do so, they compared "knockout" mice missing GIRK3 with normal mice.
The researchers found that GIRK3 knockout mice consumed much more alcohol than the control group in certain circumstances.
The results suggest that GIRK3 knockout mice drink more ethanol to boost the engagement of other neural pathways mediating alcohol's rewarding effects, the researchers noted.
Interestingly, the researchers were able to alter binge drinking in the opposite direction by injecting a GIRK3-expressing virus in the area of the midbrain called the ventral tegmental area (VTA) where a neural circuit that facilitates reward seeking originates.
Reintroducing GIRK3 in the VTA of knockout mice brought their alcohol consumption down to normal levels, and normal mice expressing more GIRK3 in the VTA drank even less. Overall, the new study showed that more GIRK3 in the VTA reduced binge drinking.
The findings appeared n the journal Proceedings of the National Academy of Sciences.
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