Anyone who attended a dazzling New Year celebration knows that a little bit of alcohol can make us euphoric, energetic and tender. But the more we drink, the more we fall into an (sometimes life-threatening) anesthetic. The scientists behind a recent study claim to have figured out how this initial buzz feels, thanks to a few drunken fruit flies.
The study, published in the Journal of Molecular Biology this month, is from researchers at The Scripps Research Institute, a nonprofit research center and graduate school located in California and Florida.
Based on previous research, the team compared the drowsiness of alcohol in the brain with that of anesthesia. Therefore, they decided to study closely a molecular pathway that activates in nerve cells when we drink alcohol or undergo sedation involving the enzyme phospholipase D2 or PLD2. It is believed that PLD2 contributes to the binding of ethanol molecules to the fat stored in the membrane or surface of nerve cells. And they used fruit flies as placeholders for humans because, remarkably, flies seem to behave the way we do when they absorb.
"They behave like humans," wrote senior author Scott Hansen, professor of molecular medicine at Scripps, said in a statement. "You lose the coordination. They literally get drunk. "
Hansen and his team put flies in a small tube and fed them with liquid food that was filled with alcohol, and the flies were buzzing as expected. When they looked at the brain of these flies, they found that activation of PLD2 via alcohol led to a chain reaction of other processes in the nerve cells. In particular, PLD2 breaks down alcohol into other molecules or metabolites, and one of these metabolites is a molecule consisting of fat and alcohol called phosphatidylethanol (PEtOH). The accumulation of PEtOH, in turn, seems to make nerve cells easier to shoot, which means their brain becomes hyperactive.
"With hyperactivity, you see the flies running around more, and that's what we equate with buzzing," said Hansen.
Hansen and his team also created flies with the gene that allowed their brain cells to recognize that PLD2 was off. In contrast to the unaltered flies, these flies did not behave at all, supporting their case that PLD2 plays a crucial role in creating the initial sense of drunkenness.
The results are particularly interesting as the authors call alcohol It is widely believed that brain cells are directly affected. However, this would be an example of the drug that indirectly affects cells via the PLD2 pathway. This is important because we are obviously interested in stopping the worst effects of alcohol in humans. It is therefore possible that medications that one day can safely interact with PLD2 will prevent us from getting drunk. This could help people who are involved with alcohol dependence. Perhaps stopping PLD2 could even prevent other negative aspects of alcohol consumption, such as a brutal hangover.
"It has definitely led to different ways of thinking about alcohol poisoning at the molecular level," said Hansen. "Most scientists thought alcohol has a direct effect. Blocking the enzyme in flies indicates that this is unlikely to be the case. "
Fruit flies are a practical substitute for humans, but their brains do not resemble ours, of course. So much more work is needed to find out if PLD2 also plays a key role in making people sing. Hansen and his team continue to explore the importance of PLD2 in producing the other notorious effects of alcohol, including sedation.
[Journal of Molecular Biology via Scripps]