Decoded! Why some casual drinkers turn into heavy alcoholics
Scientists found that selectively lesioning or ablating the NTS neurons in the specific brain region, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol
Don't just blame it on his friends if your hubby has suddenly started drinking more in recent times as scientists have now discovered neurons in a specific brain region that might be responsible for triggering a sudden uptick in alcohol consumption.
Researchers have long known that a region of the brain called the central nucleus of the amygdala (CeA) plays a role in behaviours related to alcohol use and consumption in general. Now, a team at the University of North Carolina's school of medicine has found a specific neural circuit that, when altered, caused animal models to drink less alcohol.
"The fact that these neurons promote reward-like behaviour, that extremely low levels of alcohol consumption activate these cells, and that activation of these neurons drive alcohol drinking in animals without extensive prior drinking experience suggests that they may be important for early alcohol use and reward," elaborated senior study author Zoe McElligott, assistant professor of psychiatry and pharmacology.
"By understanding the function of this circuit, we can better predict what happens in the brains of people who transition from casual alcohol use to subsequent abuse of alcohol, and the development of alcohol use disorders". McElligott investigated if a population of neurons that express a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviours and alcohol drinking.
She was especially interested in these neurons in the context of inexperienced alcohol use, such as when a person first begins to drink alcohol. Also, NTS neurons are a subpopulation of other neurons in this brain region that has been implicated in anxiety and fear.
Using modern genetics and viral technologies in male mice, McElligott and colleagues found that selectively lesioning or ablating the NTS neurons in the specific brain region, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol.
This manipulation did not either alter anxiety-like behaviour or affect the consumption of other palatable liquids such as sucrose, saccharin and bitter quinine solutions.
"We found that these NTS neurons in the central nucleus of the amygdala (CeA) send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem," McElligott explained.
Using optogenetics -- a technique where light activates these neurons -- the researchers stimulated the terminal projections of the CeA-NTS neurons in the parabrachial and found that this stimulation inhibited the neurons in the parabrachial.
"Furthermore, when we stimulated this projection, animals would drink more alcohol as compared to when they had an opportunity to drink alcohol without laser stimulation," McElligott said in a paper published in the Journal of Neuroscience.
The team hopes to explore how alcohol experience may change these neurons over time. Would these cells respond differently after animals have been drinking high quantities of alcohol over time?
"We also want to discover which populations of neurons in the parabrachial are receiving inputs from these neurons. Fully understanding this circuit could be the key to developing therapeutics to help people with alcohol use disorders," said the researchers.
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