Researchers altered the gene for a human
brain ion channel, put it in place of a worm’s version of the channel, and
observed resistance to drunkenness among the worms.
by John
Tyburski
Copyright © Daily
Digest News, KPR Media, LLC. All rights reserved.
People fond
of saying, “I’d rather have a bottle in front of me than a frontal
lobotomy” may now have a glimmer of hope for one day lowering their dependence
on alcohol with a new approach. While the pharmaceutical potential of a new
research finding is not known, authors speculate that their work paves the way
for further development.
Researchers
at the University of Texas report this week in
the Journal of Neuroscience that single amino acid change in
an important brain protein protects against drunkenness. The scientists
designed a mutated gene that encodes for the human BK channel, or “Big
Potassium” channel, and placed it into a model organism called Caenorhabditis
elegans. The nematode worm model is very popular among laboratory-based
molecular biologists and geneticists.
Once the C.
elegans worms had the mutated human BK channel instead of their own version of
the crucial protein, they could tolerate alcohol exposure without showing signs
of intoxication. Meanwhile, worms having only normal BK channels responded to
alcohol with slower movements and inhibited egg-laying, among other
intoxication indicators.
“This is the
first example of altering a human alcohol target to prevent intoxication in an
animal,” said corresponding author Jon Pierce-Shimomura in a statement.
Pierce-Shimomura is an assistant professor in the university’s College of
Natural Sciences and Waggoner Center for Alcohol and Addiction
Research.
A profound
aspect of this research is that the mutated BK channels function exactly like
their unaltered counterparts except in their response to alcohol.
“We got
pretty lucky and found a way to make the channel insensitive to alcohol without
affecting its normal function,” said Pierce-Shimomura.
The BK
channel is important in regulation of the activity of neurons, blood vessels,
and cells in the respiratory tract and urinary bladder. None of these functions
appear to be altered by the mutation engineered by Pierce-Shimomura and
colleagues.
“Our
findings provide exciting evidence that future pharmaceuticals might aim at
this portion of the alcohol target to prevent problems in alcohol abuse
disorders,” said Pierce-Shimomura. “However, it remains to be seen which
aspects of these disorders would benefit.”
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