Alcohol consumption alters the structure and function of neurons in an area of the brain called the dorsomedial striatum, find scientists.
The scientists say they "have pinpointed a population of neurons in the brain that influences whether one drink leads to two, which could ultimately lead to a cure for alcoholism and other addictions."
The study has been published in The Journal of Neuroscience by researchers from the Texas A&M Health Science Center College of Medicine in Bryan.
The dorsomedial striatum is a region of the brain that drives goal-directed behaviors, and alcohol resulted in "persistent alterations of neuronal morphology" there. The study concludes:
"Furthermore, we show that these alterations occur only in a subpopulation of neurons that positively control reward and reinforcement of drugs of abuse."
The authors raise prospects of a drug treatment for alcoholism:
"Finally, we report that blocking the activity of this neuronal population reduces alcohol intake."
Co-authored with researchers from the University of California-San Francisco (UCSF), the animal study determined that alcohol changes the physical structure of medium spiny neurons - the main type of cell in the striatum.
These neurons can either facilitate or inhibit the performance of specific behaviors because of one of two types of dopamine receptor: 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.
Periodic consumption of large amounts of alcohol acts on D1 neurons, the team found, making them much more excitable, and therefore activated with less stimulation.
"If these neurons are excited, you will want to drink alcohol. You'll have a craving," explains Dr. Jun Wang, lead author and an assistant professor in neuroscience and experimental therapeutics.
Physical changes to nerves
The changes in activation of D1 neurons could be related to physical changes at the sub-cellular level. They had more branching and a greater density of the mature, mushroom-shaped spines in alcohol-exposed mice than in the abstaining counterparts.
Those mice not exposed to alcohol had more of the immature versions of the mushroom-shaped spines in D1 neurons of their brains.
Introducing the study in the journal, Teresa Esch, PhD, explains:
"These data suggest that heavy alcohol consumption induces plasticity of glutamatergic synapses in D1-MSNs, but not in D2-MSNs of the dorsomedial striatum. This plasticity may promote further alcohol consumption." She adds:
"Consistent with this hypothesis, infusion of D1 dopamine receptor antagonists into the dorsomedial striatum of alcohol-consuming mice reduced subsequent alcohol intake, whereas D2 dopamine receptor antagonists did not."
The "much-reduced desire to drink alcohol" in the animal models given a drug to at least partially block the D1 receptor was perhaps the most exciting finding, say the researchers.
"If we suppress this activity," says Dr. Wang, "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."
Dr. Wang adds: "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."