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A robust study conducted by researchers at Linköping University has uncovered a molecular mechanism in the brain that is considered essential to the development of alcohol dependence. The research potentially explains why some people are more prone to alcoholism than others and may even lead to a new drug treatment that could treat alcohol dependence.
"We must understand that one of the main features of addiction is that you know that it will harm you or even kill you, and that something is wrong with the motivational control and that you continue to do it, "says Markus Heilig, co-author. lead the new study.
Thus, researchers have begun to better understand what is happening in the brain that leads to a choice despite the negative consequences. An experiment was set up with rats where animals were given the choice between sugar water and alcohol. The alcohol, triggered by pressing a lever, was harder for animals to access than sugar water.
After a period of time, it was observed that only about 15 percent of the rats continued to work harder to get the alcohol on the sugar water. Interestingly, researchers note that this percentage is similar to the amount of humans suffering from alcohol dependence. When the scientists added a small electric shock to the lever supplying alcohol, they observed that the rats were still searching for the substance.
So what was different between the rats that searched for alcohol despite the negative consequences and the rats that did not have it?
After measuring the expression of hundreds of specific genes in alcoholic rats, the researchers focused on a particular gene. Located in the amygdala, a region of the brain previously implicated in alcohol dependence, this gene is known to regulate a protein called GAT-3. In rats predisposed to alcoholism, the expression of this gene was significantly lower than normal, and subsequently, GAT-3 levels were significantly lower than normal. Going even further, the researchers selectively eliminated the expression of GAT-3 in rats that had previously chosen sugar water rather than alcohol.
"Decreasing the expression of the carrier had a noticeable effect on the behavior of these rats: animals that had preferred the sweet taste to alcohol reversed their preference and began to choose alcohol" explains Eric Augier, principal researcher of the project.
Finally, the study sought to find some correlation in human subjects by examining levels of GAT-3 in tonsil tissue samples from people who died with alcohol dependence diagnosed. Interestingly, the results confirmed that these subjects with alcoholism actually had lower GAT-3 levels than normal human subjects.
"It's one of those relatively rare times when we find an interesting change in our animal models and we see the same change in the brains of human alcoholics," says Dayne Mayfield, co-author of the new study. "This is a very good indication that our animal model is correct, and if our animal model is correct, we can select therapeutics and increase confidence in the results."
One thing that is not clear at this point is what leads to a person developing lower levels of GAT-3. This could be simply genetic, or it could be a more complex set of environmental factors that stimulate a deficiency of this neurological mechanism. In one way or another, it is an impressive research work that adds weight to the argument that alcohol dependence does not exist. Is not a psychological condition, but a more complete neurological disease.
The study was published in the journal Science.
Source: Linköping University
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