Scripps
Research Institute Study Links Brain Protein to Binge Drinking
By Dr.Fourkan Ali
Binge
drinking is defined by heavy consumption of alcohol over a short period of time
in order to reach intoxication.
Scientists at the Scripps Research Institute have discovered the
key role a brain protein plays in controlling binge drinking. When they deleted
the gene for this protein in mice, it ramped up the alcohol consumption of the
rodents and prevented the brain from signaling the rewarding properties of alcohol.
Published in the journalProceedings of the National Academy of
Sciences, the study could play
a major role in the development of medications and medical procedures to
address binge drinking behaviors in alcoholics.
Characterized by heavy episodic drinking, binge drinking is
defined by heavy consumption of alcohol over a short period of time in order to
reach the point of intoxication. According to the U.S. Centers for Disease
Control and Prevention, binge drinking puts people at greater risk for health
problems such as cardiovascular disease, liver disease, and neurological
damage.
"Alcohol hits a lot of different targets in our brain,
which makes disentangling the in vivo effects of alcohol quite
complicated," explains TSRI biologist Candice Contet, senior author
of the study. "Our study sheds light on the molecular mechanisms
implicated in binge drinking."
The goal of the new study was to identify the role of a member
of the "G protein-gated inwardly rectifying potassium channel" (GIRK)
family in the behavioral and cellular responses to alcohol.
Distributed throughout the nervous system, GIRK channels
decrease the excitability of neurons, making them less likely to fire. Alcohol
can directly activate GIRK channels. Scientists did not know, however, whether
this action was directly connected to the behavioral effects of alcohol.
In the new study, Dr. Contet and her colleagues decided to focus
on the GIRK3 subunit, which had previously been shown to modulate the effects
of other drugs, such as the "date rape drug" γ-hydroxybutyrate (GHB)
and cocaine. The researchers investigated how GIRK3 influenced mouse behavior
and neuronal function in the presence of alcohol. To do so, they compared
"knockout" mice missing GIRK3 with normal mice.
GIRK3 knockout mice and controls showed differences in alcohol
intake in a test mirroring human behavior during a "happy hour" at a
bar. In this test, mice were given access to ethanol for only two hours a day,
at a time when they were most likely to drink to the point of intoxication. The
researchers found that GIRK3 knockout mice consumed much more alcohol than the
control group.
"Mice lacking GIRK3 ... (are) drinking more because they feel
less pleasure and therefore need to drink more to reach the same level of
pleasure as normal mice," explainedContet.
A striking difference between normal and GIRK3 knockout mice
emerged in the presence of alcohol. The pleasure pathway became completely
insensitive to alcohol's activating effect without GIRK3. Alcohol also was
unable to trigger the release of dopamine in the ventral striatum of GIRK3
knockout mice. The results suggest that GIRK3 knockout mice drink more ethanol
to boost the engagement of other neural pathways mediating alcohol's rewarding
effects.
"The dramatic effect of GIRK3 deletion on the ability of
alcohol to excite VTA neurons was surprising. Even when applied at a very high
concentration, alcohol was unable to alter the firing of neurons missing
GIRK3," said research associate Melissa Herman.
The results of the study have led the researchers to believe
that a compound selectively targeting GIRK3-containing channels could prove to
be an effective treatment technique. Such a compound may hold promise for
reducing alcohol consumption in heavy binge drinkers.
Sources - The Fix
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