'Drunk Gene' in Mice May Lead to Treatment for Humans
Three or more blind (drunk) mice may yield clues to why some people struggle with alcohol abuse and others don't.
Scientists in Britain have discovered a gene mutation that regulates alcohol consumption and identified the mechanism that made the critters tipsy. The research, published today in the journal Nature and Communications, could have broader implications for alcohol dependence in humans.
An estimated 22 million Americans abuse or are dependent on alcohol, drugs, or both, according to the Substance Abuse and Mental Health Services Administration (SAMHSA). Some 54 million take part in binge drinking and 15.9 million are heavy drinkers.
"It is unlikely that a single gene can change alcoholism in humans," lead author Dr. Quentin Anstee, consultant hepatologist at Newcastle University, told ABCNews.com. "We are much more complicated in emotions and environment. It's more like a whisper in the ear that is present that makes certain life choices seem more pleasurable or easier. It causes [alcoholism] in mice and it may be an influence in humans."
Typically, mice do not like alcohol. But those with the mutation were drinking the human equivalent of one to two bottles of whiskey a day. Anstee said their next job was to find out if this research can apply to humans.
The study shows that alcohol consumption increases following mutations to the g-aminobutyric acidA receptor (GABAAR) b1 subunit gene (Gabrb1). Researchers used a mouse model that exhibited a strong genetic preference for alcohol. The results showed a "new and important link between GABAAR function and increased alcohol consumption that could underlie some forms of alcohol abuse," according to the study.
Mice with a genetic mutation to the gene Gabrb1 chose drinking alcohol over water - in fact 85 percent of the time, they preferred the spiked drinks. They voluntarily drank enough in an hour to become so drunk they had difficulty coordinating their movements, according to the study. Mice without the lush gene showed no interest in the alcoholic drinks.
The scientists also noted that the mice had to "work" for their alcoholic drinks, pushing a lever and continuing to do so even over long periods of time.
"It's amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviors like alcohol consumption," said Anstee. "We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play. But there is the real potential for this to guide development of better treatments for alcoholism in the future."
Anstee worked among a group of researchers from four other universities - Imperial College London, Sussex University, University College London and University of Dundee.
They noted that these brain changes in mice were particularly strong in the region that controls pleasurable emotions and reward.
"The mutation of the beta1 containing receptor is altering its structure and creating spontaneous electrical activity in the brain in this pleasure zone, the nucleus accumbens," said Anstee. "As the electrical signal from these receptors increases, so does the desire to drink to such an extent that mice will actually work to get the alcohol, for much longer than we would have expected."