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Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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The Frat House Mouse
19 July 2004 (All day)
For some mice, getting drunk is a lot harder than chugging a few tequila shots. Mice that lack a particular protein receptor take longer than their alcohol-swilling peers to become intoxicated. The results provide a candidate gene for alcoholism and reveal a potential mechanism for how ethanol inebriates animals.
No one knows why some people get giddy on a couple drinks while others stay sober, but those who require more libation to start dancing on tables have a higher risk of alcoholism. Alcohol boosts the amount of a brain chemical called adenosine--thought to cause the symptoms of drunkenness, including sedation--which limits the amount of alcohol one can imbibe. Booze increases adenosine by blocking a different protein receptor called ENT1, which normally transports loose adenosine back into the neuron. That means adenosine is free to whip up the woozy adenosine receptors. Chronic exposure to ethanol causes ENT1 receptors to become insensitive to alcohol and go back to cleaning up adenosine. Neurologist Robert Messing and colleagues at the Ernest Gallo Clinic and Research Center, Emeryville, California, wondered if lack of ENT1 from the get-go would make animals more tolerant to alcohol.
To find out, they genetically engineered mice to lack both copies of the gene for ENT1. The team then tested their sensitivity to alcohol by injecting the mice with enough alcohol to get them just over the legal limit. Instead of putting them in driver's seat, the researchers placed the animals on a rotating rod to check their balance. Like talented midwestern log-rollers, the mice lacking ENT1 stayed on the rod nearly twice as long as the normal mice. Both types of animals had equivalent blood alcohol levels, indicating the effect was not due to faster metabolism of the ethanol by the mutants, the team reported 18 July online in Nature Neuroscience.
Given free access, mutant mice drank twice as much alcohol as normal mice. At the same time, adenosine receptors in the mutant mice were less active. When given a chemical that stimulates the adenosine receptors, the ENT1-lacking mice reduced their consumption at happy hour to normal levels. Together, the findings indicate that under normal conditions, ENT1 makes the mice drunk by stimulating the adenosine receptors, which then slows down their drinking. Work is under way to determine if variations of ENT1 occur in the human population and if they correlate with alcohol tolerance and abuse.
The new finding makes ENT1 "really really interesting," because its activity regulates how much alcohol an animal can ingest and still stand, says psychiatrist Marc Schuckit of the San Diego Veteran's Administration Hospital. If variants of ENT1 exist naturally in the human population, they might correspond to differing amounts of consumption. The question now is whether the molecular mechanism holds up in humans. If it does, the knowledge could help design treatment strategies.