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Activating particular neurons may be a way to control alcohol-drinking, a new study suggests.

Prior research has shown that alcohol consumption alters the physical structure and function of medium spiny neurons, in the dorsomedial striatum. Essentially, this means that activation of one type of neuron, called D1, determines whether one drink leads to two. Now, scientists have discovered the ones that tell us to stop.

These neurons can be thought of like a tree, with branches, and small protrusions, or spines, coming off of them. Each neuron has one of two types of dopamine receptors—D1 or D2—and so can be thought of as either D1 or D2 neurons.

D1 neurons are informally called part of a “go” pathway in the brain, while D2 neurons are in the “no-go” pathway. In other words, when D2 neurons are activated, they discourage action—telling you to wait, to stop, to do nothing.

“At least from the addiction point of view, D2 neurons are good,” says Jun Wang, assistant professor of neuroscience and experimental therapeutics at Texas A&M University College of Medicine. “When they are activated, they inhibit drinking behavior, and therefore activating them is important for preventing problem drinking behavior.”

The trouble is, even in individuals without alcoholism, D2 neurons tend to become deactivated when we drink too much. This deactivation means there is nothing telling us to stop drinking, so we drink more, in a self-perpetuating cycle.

In animal models, repeated cycles of excessive alcohol intake, followed by abstaining from alcohol, actually change the strength of these neuronal connections, making D2 signals less powerful—which results in essentially training the individual to seek alcohol.

“Think of the binge drinking behavior of so many young adults,” Wang says. “Essentially they are probably doing the same thing that we’ve shown leads to inhibition of these so-called ‘good’ neurons and contributes to greater alcohol consumption.”

These findings provide insight into another mechanism underlying the complicated disease we call alcoholism. “Our current and previous research are essentially two sides of the same coin,” Wang says. “D1 and D2 medium spiny neurons have essentially opposing roles in alcohol consumption.”

By manipulating the activity of these neurons, the researchers were actually able to change the alcohol-drinking behavior of the animal models who had been “trained” to seek alcohol. By activating D2 neurons, they were able to decrease alcohol consumption, and the more the D2 neurons were activated, the greater the effect is likely to be.

Although Wang cautions the work is still a long way from human testing, in theory, if scientists could someday use drugs or electrical stimulation or some other method of activating the D2 neurons—these so-called “no-go” neurons—then we might be able to prevent alcoholics from wanting another drink, Wang says.”That’s the ultimate goal.”

The findings appear in the journal Biological Psychiatry. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) supported the work.

Source: Texas A&M University