“Maybe just one more.”
We’ve all been there—you’re craving that next slice of pizza, another cookie, maybe another bowl of kettle chips at a friend’s get-together. For those in the recovery community, a past life of pints of beer, another “hit” or “drop”, or perhaps another plunge of the syringe is what comes to mind. Whatever it is, the fact remains that there’s an itch seemingly attracting us to an abyss of literal impairment of the mind and, in time, of the body. It’s hard to fight an enemy we do not understand, especially when that enemy is oneself, a puppet of some outside force. Fortunately, researchers from the Texas A&M Health Science Center College of Medicine in Bryan may have helped to shed some light on the monkey clinging to our backs: the culprit in question is what is referred to as the dorsomedial striatum region of the brain, and it drives goal-directed behaviors.
According to the study, published in The Journal of Neuroscience, alcohol’s effect on this part of the brain triggered “persistent alterations of neuronal morphology” in a very specific collection of neurons which positively controls reward and reinforcement of drugs of abuse. Blocking activity in this subpopulation of neurons has the effect of diluting the cyclical use-reward-use mentality that many of us experience when we struggle with that “one last drink.” In essence, researchers may have found a way to put a stop-gap between the individual and addiction, and not just of alcohol and drug abuse.
The study was completed with the collaboration of researchers from the University of California, San Francisco. When working with animals, it was determined that alcohol changed the physical structure of medium-sized spiny neurons, which make up the main type of cell in the striatum and “either facilitate or inhibit the performance of specific behaviors because of one of two types of dopamine receptors: D1 or D2. D1 neurons are informally called part of a ‘go’ pathway in the brain, while D2 neurons are in the ‘no-go’ pathway.”
The “Go” neuron is only every activated once an individual consumes copious amounts of alcohol, but when he or she does, the neurons there are much more easily “activated” the less that person drinks over time.
As Dr. Jun Wang, lead author and an assistant professor in neuroscience and experimental therapeutics puts it, via Medical News Today:
“If these neurons are excited, you will want to drink alcohol. You’ll have a craving.”
Exciting the researchers even more was the introduction of a drug whose purpose was to partially block the D1 receptor. Dr Wang continues:
“If we suppress this activity, we’re able to suppress alcohol consumption. This is the major finding. Perhaps in the future, researchers can use these findings to develop a specific treatment targeting these neurons.
My ultimate goal is to understand how the addicted brain works, and once we do, one day, we’ll be able to suppress the craving for another round of drinks and, ultimately, stop the cycle of alcoholism.”
On a final note, perhaps one shouldn’t be so quick to dismiss our earlier, prematurely facetious examples on overeating—this study could very well spell the end of overconsumption as a whole. That being said, the immediate concern that comes to mind when touching on the subject of a general area that covers such a wide swathe is whether being treated for alcoholism will inadvertently inhibit already normal eating patterns (or if drinking habits will be worse than before following termination of treatment). Only time will tell.
What do you think?