Researchers have identified a gene mutation that regulates alcohol consumption and when faulty leads to excessive drinking.
In a study conducted on mice, researchers found that the subjects generally preferred a normal bottle of water to a bottle of diluted alcohol. However, mice with a genetic mutation to the gene Gabrb1 overwhelmingly preferred drinking alcohol over water, according to a press release. Mice with the gene mutation chose 85 percent of their daily liquid consumption in the form of alcohol beverages, with alcohol strength being as much as that of wine.
"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," Dr Quentin Anstee, Consultant Hepatologist at Newcastle University, joint lead author said in the statement. "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."
For the study, Anstee and a team of researchers from Imperial College London inserted subtle mutations into the genetic code throughout the genome of mice randomly and then tested them for alcohol preference. Researchers noticed that the gene Gabrb1 changed alcohol preference in mice so strongly that the ones carrying either of the single base-pair point mutations in this gene chose drinking alcohol over water.
Researchers also found that mice with this mutation were willing to work even harder to get alcoholic drinks than mice, which preferred water. The mice were seen pushing levers for long periods of time just to attain their alcoholic drink. They would drink sufficient alcohol to get intoxicated in an hour, which would result in them becoming clumsy coordinating their movements.
Anstee and his team then tracked down the cause of this excessive drinking to single base-pair point mutations in the gene Gabrb1, which codes for the beta 1 subunit, an important component of the GABAA receptor in the brain. GABAA responds to the brain's inhibitory chemical messenger (GABA) to regulate its activities. Even in the absence of GABA, researchers found that the gene mutation caused the receptor to activate spontaneously.
This activation was strong mostly in the nucleus accumbens, which is the region of the brain that controls satisfying emotions and rewards.
"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," Anstee explained. "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."
Findings of the study were published in the online journal Nature.
