Binge drinking brain switch identified by scientists

LINKÖPING, Sweden — A neural switch that triggers compulsive drinking has been discovered in the brain. Researchers from Linköping University in Sweden say a small group of nerve cells makes some people more likely to binge on wine, beer, or spirits – even when they’ve had enough.

The discovery opens the door to new drug therapies that combat alcohol abuse disorder.

“We discovered that a small group of nerve cells in a small region of the brain are the difference between being able to put the brakes on in a normal manner, as most of our rats did, and not being able to stop yourself,” says study leader and psychiatrist Professor Markus Heilig, in a university release.

According to the CDC, excessive alcohol use contributes to more than 95,000 deaths in the United States every year. While many people enjoy a regular drink without ill effects, others succumb to addiction and don’t know how to stop.

The discovery of these cells could lead to an effective treatment for problem drinkers – half of whom scientists say have a genetic predisposition to drink heavily.

“I had not expected that such a small group of nerve cells would be so decisive for this complex behavior. And I could not have imagined that it would be possible to demonstrate so clearly, by manipulating these cells from outside, that they cause the behavior,” Prof. Heilig says.

Some people lack the ‘brake’ to pass on alcohol

The Swedish team pinpointed a mechanism in the middle of the amygdala – an area of grey matter linked to reward – known as PKCδ-positive nerve cells. The cells fuel alcohol consumption in susceptible rodents despite negative consequences, a phenomenon called “compulsive use.”

Making decisions, such as whether to take another drink, is complex. The brain has a system that values pleasures such as tasty food, sex, and drugs and drives people to seek more. It also contains a “brake” to balance the pros and cons however, this system fails in heavy drinkers.

When scientists turned the neurons off using state-of-the-art molecular methods, the animals’ ability to refrain returned. The enzyme PKCδ played the key role – offering hope of developing medications that target this region. In the study, published in Science Advances, rats learned they could press a lever to obtain a small amount of alcohol.

After a period, the conditions changed, such that they received an electric shock together with the alcohol. In this case, most rats stopped. However, the brake failed to function in around one-in-three mice. These animals continued to keep taking drinks despite their behavior now causing discomfort.

A marker that forms in triggered nerves lit up cells across the brain. The hub was tracked to the central amygdala, which is involved in learning mechanisms coupled with fear.

The brain switch controls other compulsive behaviors

Three years ago, the researchers showed choosing alcohol over another reward is also controlled by these nerve cells. The scientists could switch the behavior on and off by manipulating molecular mechanisms in this part of the brain.

Recent research by other scientists suggests humans and animals fall into two groups regarding reward-seeking behavior. They can either put the brake on it when it may have negative consequences or not. Prof. Heilig is calling for further investigations into clinical markers that can reveal whether a person has an individual vulnerability to addiction. Early discovery may make it possible to create new preventive measures for problem drinkers.

“We must understand that the inability to brake behavior that is becoming detrimental is an important risk factor, and also maintains addiction once it has developed. We must reinforce the ability to brake alcohol-seeking activity in people who run an increased risk of developing addiction, not only by working with their behavior but also by developing medications that target the molecular mechanisms behind the behavior,” Prof. Heilig concludes.

South West News Service writer Mark Waghorn contributed to this report.

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