Scientists discover neural circuit responsible for alcohol consumption


Washington D.C.: Scientists have 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. They have now found a specific neural circuit that when altered caused animal models to drink less alcohol.

The study was published in the Journal of Neuroscience.

According to senior author, Zoe McElligott, PhD, assistant professor of psychiatry and pharmacology, “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.”

“It’s our hope that 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 added.

Using modern genetics and viral technologies in male mice, McElligott and colleagues found that selectively lessening the NTS neurons ( specific neuropeptide which contributes to reward-like behaviours and alcohol drinking) in the CeA, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol.

This manipulation did not alter anxiety-like behaviour. It also did not affect the consumption of other palatable liquids such as sucrose, saccharin, and bitter quinine solutions.

“We found that these NTS neurons in the CeA send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem,” McElligott said.

“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 contrast to our study where we ablated the NTS neurons, laser stimulation of this parabrachial pathway also caused the animals to consume caloric and non-caloric sweetened beverages. When the animals were presented with regular food and sweet food, however, laser stimulation did not enhance the consumption regardless of the mouse’s hunger state.

This suggests that different circuits may regulate the consumption of rewarding fluids and solids.”

McElligott and her graduate student Maria Luisa Torruella Suarez, the first author of this study, hope to explore how alcohol experience may change these neurons 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 the therapy to help people with alcohol use disorders.” (ANI)