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Scripps Research scientists have discovered that they can turn the tide
desire to drink in alcohol-dependent rats, in a jiffy.
The researchers were able to use lasers to temporarily inactivate a
specific neuronal population, by reversing the alcohol-seeking behavior and
even by reducing the physical symptoms of withdrawal.
"This discovery is exciting – it means we have another piece of the puzzle to explain the neural mechanism that leads to alcohol consumption," says Olivier George, PhD, badociate professor at Scripps Research and lead author of the new study, published in the newspaper Nature Communications.
Although the laser treatment is far from ready to be used by humans, George
believes that the identification of these neurons opens the door to drug development
therapies or even gene therapies for alcohol dependence.
"We need compounds specific to this neural circuit," says George.
According to the National Institute of Fight against Alcohol Abuse and Alcoholism,
In the United States, more than 15.1 million adults suffer from alcohol
use the mess. Previous work at Scripps Research has shown that
the transition from an occasional consumption to a dependent consumption takes place
next to the fundamental changes in the way the brain sends signals. These
signals cause intense cravings that make it so difficult for many
people to reduce their consumption of alcohol.
George and his colleagues were looking for brain cells that
impaired driving by alcohol In 2016, they
reported finding a possible source: a neuronal "set"
or group of connected cells in a region of the brain called the central nucleus
of the amygdala (CeA). This discovery marks a major advance in cartography
the brain but the researchers had to characterize the identity of
the neurons of this set.
For the new study, they tested the role of a subset of neurons in
together, called neurons corticotropin releasing factor (CRF). the
George lab had found that these CRF neurons account for 80 percent of
l & # 39; together. Were these neurons the brain of alcohol?
cravings?
The researchers studied these neurons using optogenetics, a
technique that involves the use of light to control cells in life
fabric. The rats used in this study were implanted surgically with a
fibers were intended to shed light on CRF neurons – to inactivate them at
the switchover of a switch.
First, scientists have established a baseline to determine how many rats
drink before being addicted to alcohol. Rats drank little
this point – the equivalent of a glbad of wine or a beer for a human.
Scientists then spent several months increasing consumption in these
rats to establish alcohol dependence.
The researchers then removed the alcohol, which resulted in
symptoms in rats. When they offered alcohol again, the rats drank
more than ever. The CeA neural set was active and told the rats
drink more.
Then scientists switched to lasers to disable the CRF
neurons – and the results were dramatic. The rats are immediately returned to
their pre-dependent consumption levels. Intense motivation to drink
was gone. Inactivate these neurons also reduced the physical effects
withdrawal symptoms, such as abnormal gait and tremors.
"In this multidisciplinary study, we were able to characterize,
target and manipulate a critical subset of neurons responsible for
excessive consumption, "says Giordano de Guglielmo, PhD, first author of
the Scripps Research and Scripps Research Scientist. "It was a team
effort, and while we used difficult techniques, working with experts
on the ground and with the right tools, has made everything easier and
pleasant."
The effect was even reversible. Turn off the lasers and the rats have resumed their dependent behavior.
From the point of view of basic science, this progress is enormous:
reveals the cabling in the brain that drives a specific, destructive
behavior. George says the next step in translating this work to man
is to find a way to selectively inhibit only these specific CRF neurons,
maybe using a new or recycled compound identified using
high throughput screening of large libraries of compounds.
Meanwhile, de Guglielmo plans to take a closer look at the signage
brain pathways affected by the deactivation of CRF neurons.
New study shows reduction in consumption is linked to CRF neurons
who send projections to reach another area of the brain called the bed
nucleus of the terminal streak. De Guglielmo thinks of other projections
of these neurons can have different roles in alcohol dependence. It is
also interested in identifying the role of these brain circuits in
opioid dependence.
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