For many people, the dividing line between casual, social drinking, and alcoholism is the ability to stop consuming alcohol before it becomes too much. Addiction experts might suggest that’s an oversimplified version of addiction and they’d be right.
There are other factors, such as genetic predisposition or neurochemical imbalances, which play a large role in the disease of alcoholism.
Now, a study conducted in the Department of Neuroscience and Therapeutics College of Medicine at Texas A&M Health and Sciences Center, has likely uncovered yet another layer in the brain’s complex neurological response to alcohol.
Published in the journal Biological Psychiatry’s May 2016 issue, scientists report that the decision to continue drinking adult beverages, even if we’ve had too many already, boils down to two neurons in the brain. Both neurons are not surprisingly located in the decision-making part of the brain, a region called the dorsomedial striatum.
What Neurons in the Brain Signal to Stop Drinking Alcohol?
- When activated, the first neuron, D1 or what researchers refer to as the “go” pathway, determines whether a person goes from one drink to the next to the next and so on
- Activation of the D2 neuron, the “no-go” pathway, is what signals a person to cease alcohol consumption
Alcohol abuse alters the brain’s capability to process dopamine, a neurological chemical responsible for feelings of pleasure. This is why alcoholics have to drink more to get drunk.
Prolonged alcoholism also erodes the D1 neuron or “go” pathway, which is one of the receptors dopamine binds to. Put together, these facts shed a physiological light on why moderate amounts of alcohol don’t satisfy people suffering from alcoholism.
“At least from the addiction point of view, D2 neurons [or the “no-go” pathway] are good,” said Dr. Jun Wang, one of the study’s author’s, in a statement corresponding with the release of the study.
Though the study was performed on mice and human testing will eventually follow, scientists are encouraged by the findings. Research has already shown, in the brains of deceased alcoholics, that D2 neurons weaken once alcohol changes the chemical structure of the brain’s reward system.
From a neurological standpoint, there are very few (if any) signals sent telling a person to stop drinking.
Using that knowledge, Wang and her colleagues stimulated the “no-go” pathway in rodents trained to seek alcohol. The result was a substantial decrease in alcohol seeking behavior.
What’s Next For the D2 Neuron Study?
Though she acknowledges that science is a ways off from a practical application for this discovery, Wang believes that eventually a method of stimulating D2 neurons of the “no-go” pathway” in alcoholics, with medication or electrical stimulation or an as of yet unknown method, might diminish their desire for another drink.
“That’s the ultimate goal,” Wang said in her statement. “I hope these findings will eventually be able to be used for treatment of alcohol addiction.”
Findings such as these, even without a magic pill to solve the problem, reinforce the fact that addiction is a chronic neurological disease and not just a lack of willpower on the part of the afflicted drinker.
In fact, evidence of this nature suggests that some people might not be capable of deciding when enough is simply enough.