U.S. researchers have developed "mutant worms" that do not get drunk by alcohol, a breakthrough that could lead to new treatment for people trying to quit drinking. Neuroscientists from the University of Texas injected a "modified human alcohol target" into the Caenorhabditis elegans worm, changing the animal's neuron channels to block the inebriating effects of alcohol. Metro asked neuroscientist and study author Jon Pierce-Shimomura whether humanity will soon be able to sober up in a second.
What was the point of your study?
Researchers are trying to find ways to prevent alcohol from changing brain function that leads to alcohol abuse behaviors such as intoxication, tolerance, craving and addiction. One way to do this is identify how alcohol acts on important molecular targets in the brain. We found that one conserved target, a neuron channel called the BK channel (found both in worm and human), is required for inebriation to happen. Our study is exciting because it suggests a way to block alcohol from acting on this channel.
How did you get the worms intoxicated?
We harvested them on agar-filled plastic plates. To get them drunk, we soak the agar with alcohol – essentially Jello shots – and then put the worms on. They got drunk within five minutes. Like in humans, alcohol slows down or stops most basic behaviors of the worm. It slows its crawling, making it looks very flaccid, and prevents it from laying eggs. We specifically chose the Caenorhabditis elegans, worms because they model intoxication well.
Then how did you reverse the effects of getting tipsy?
We altered the BK channel, which regulates activity of neurons, blood vessels, the respiratory tract and the bladder. We got pretty lucky and found a way to make the channel insensitive to alcohol without affecting its normal function. Our findings that prevent an alcohol-BK channel interaction provides a promise that a hypothetical drug may be developed without seriously affecting human health.
When will this sobering treatment be available for humans?
In science, often the hardest part is gathering the first evidence that such a science-fiction idea is possible. Our study provides the first proof of this possibility. Interestingly, the research lab in Tennessee independently discovered that a mutation in a nearby portion of a mouse's BK channel has a similar effect when studied at the single-molecule level. Together, our results signal the start of a race to invent such a drug.