It looks like you're new here. If you want to get involved, click one of these buttons!
If you can read this message, please contact us immediately at the following email address:
We'd like to communicate.
A study, published this week in The Journal of Neuroscience, built on previous work on a certain subset of neurons that seem to play a substantial role in alcoholism.
The neurons in question make up just 5 percent of the total neurons in the amygdala and are referred to as the central nucleus of the amygdala; this subset of neurons have been shown to become activated by frequent alcohol use. The more an individual drinks, the more the neuronal circuit is reinforced. This then drives further alcohol use and addiction.
Researchers from The Scripps Research Institute (TSRI) set out to see if this neuronal group could be influenced and perhaps controlled.
To this end, lead author Giordano de Guglielmo designed a rat model in which the alcohol-activated neurons express a specific protein. This gave the team a unique ability to observe how these neurons behaved. Without the protein label, alcohol-linked neurons are very difficult to identify.
Once the specific neurons were labeled in this way, the researchers
injected a compound that could inactivate only the alcohol-linked
neurons. The neurons were effectively silenced, and the results were
Much to the researchers' surprise, the rats completely stopped compulsively drinking alcohol. The change was not momentary, either, it lasted for as long as the rats were monitored.
Because the response was much stronger than expected, the team went on to run the experiment a second and third time to check the findings; each time, the results were the same. Once the specific amygdala neurons were silenced, the need for alcohol evaporated. As study leader Olivier George says: "It's like they forgot they were dependent."