Easily accessible and highly habit-forming, alcohol is now one of the world’s most addictive substances, with roughly two billion individuals worldwide consuming it and three million associated with its misuse annually. As alcohol alters a variety of neurological processes, from molecular biology to cognition, research has focused on the identification of brain mechanisms supporting the reinforcement of alcohol dependence and the progression of changes in neural function induced by chronic ethanol consumption. Now, a study from researchers at the UNC School of Medicine shows alcohol consumption is regulated by the activity of a particular network of neurons in a specific brain region. The team states their discovery could lead to a better understanding of why some casual drinkers develop an alcohol use disorder. The study is published in the journal Neuroscience.
Previous studies show addictive behavior associated with alcoholism is characterized by compulsive preoccupation with obtaining alcohol, loss of control over consumption, and development of tolerance and dependence, as well as impaired social and occupational functioning. Like other addictive disorders, alcoholism is characterized by chronic vulnerability to relapse after cessation of drinking. It has been shown 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. However, it’s still unclear which precise networks of brain cells mediate these behaviors. The current study investigates if a population of neurons in the CeA expressing a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviors and alcohol drinking.
The current study utilizes modern genetic and viral technologies in male mice to show selectively ablating the NTS neurons in the CeA, while maintaining other types of CeA neurons, causes the animals to drink less alcohol. Results show this manipulation did not alter anxiety-like behavior and did not affect the consumption of other palatable liquids such as sucrose, saccharin, and bitter quinine solutions. Data findings show NTS neurons in the CeA send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem.
Results show optogenetic stimulation of projections from these neurons to the parabrachial nucleus is reinforcing and increases ethanol drinking as well as consumption of sucrose and saccharin solutions. The lab states this suggests the central amygdala to parabrachial nucleus projection influences the expression of reward-related phenotypes and is a novel circuit promoting the consumption of ethanol and palatable fluids. They go on to add when the animals were presented with regular food and sweet food, optogenetics did not enhance the consumption regardless of the mouse’s hunger state. They conclude different circuits may regulate the consumption of rewarding fluids and solids.
The team surmises they have identified a specific neural circuit that can be altered to reduce the alcohol intake in animal models. For the future, the researchers state by understanding the function of this circuit, it can be better predicted what happens in the brains of people who transition from casual alcohol use to the abuse of alcohol, and alcoholism.
Source: UNC School of Medicine
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