ARTICLE
Scientists have known that a region of the brain called the central nucleus of the amygdala (CeA) plays a role in behaviors related to alcohol use and consumption in general. It's been less known which precise populations of brain cells and their projections to other brain regions mediate these behaviors. Now, scientists have discovered that specific neurons in the CeA contribute to reward-like behaviors, alcohol consumption in particular. This research pinpoints a specific neural circuit that when altered caused animal models to drink less alcohol. "The fact that these neurons promote reward-like behavior, 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," said the senior author. "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.” Researchers set out to investigate if a population of neurons that express a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviors and alcohol drinking. 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. When the scientists stimulated this projection with a laser in one half of the animal's box, animals would spend more time where the stimulation would occur. Animals also learned to perform a task to get the laser stimulation to turn on, and they would do this repeatedly, suggesting that they found this stimulation to be rewarding. "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. 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 a 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.” Source: https://www.sciencedaily.com/releases/2019/12/191212122550.htm