The National Institute on Drug Abuse, NIH, defines addiction as “a chronic, relapsing brain disease characterized by compulsive drug seeking and use, despite harmful consequences.” The definition becomes murky as scientists attempt to unravel the brain and explore the biology of the brain that is behind this behavior.
Before biologically discussing why a person becomes addicted, it is important to discuss the factors that determine whether a person becomes addicted. Every person makes a decision by initially choosing to try drugs or alcohol. Brain imaging studies have shown physical changes in regions of the brain responsible for judgment, decision making, learning and memory, and behavior control after continual substance use. The question that remains is why and how do some brains become altered while others do not?
While the NIH maintains that the answer to this question varies on an individual basis, it does cite 6 risk factors that increase the chances a person will develop an addiction, as well as 6 protective factors that decrease these same chances. Risk factors include aggressive childhood behavior, lack of parental supervision, poor social skills, drug experimentation, accessibility to drugs at school, and poverty levels.
While these factors alone cannot serve as predictors of addiction, there is a correlation between the amount of risk factors a person has and her chances of becoming addicted. Protective factors that have been correlated with lower chances of the development of addiction include good self- control, parental presence, positive relationships, academics, school drug policies, and good surroundings. The other important factors at play are an individual’s genetic predisposition to addiction as well as the environmental factors contributing to the expression of these genes, which the NIH cites as being as high as 40-60% of an individual’s overall vulnerability to addiction.
Understanding the biology of the brain is crucial in this discussion. The three areas of the brain that are involved are the brain stem’s control of critical bodily functions, the limbic system’s control of the reward system, and the cerebral cortex’s control over our senses and decision making. Neurons communicate between brain regions by using electrical signaling as well as chemical signaling by way of neurotransmitters. It is known that substances, including alcohol, interfere with the brain’s chemical signaling by either causing a release of higher amounts of natural neurotransmitters or by interfering with the brain’s neurotransmitter recycling system.
Dopamine, a neurotransmitter involved in the pleasure center of the brain, has long been implicated in addiction. In the general addiction model, the substance being used causes an increase in dopamine levels, which produces a pleasurable effect. Eventually, an individual develops a tolerance towards the drug, meaning she must use greater amounts of the drug in order to produce the same level of pleasure. While scientists have unraveled much about the brain in recent years, much about the “drinking” brain is currently being uncovered.
Jun Wang, an assistant professor in the Department of Neuroscience and Experimental Therapeutics at Texas A&M College of Medicine, and his research lab recently published their findings on how drinking alcohol alters the brain structure, specifically focusing on the neurons in the dorsomedial striatum, a region of the brain’s reward system. This region is filled with two types of medium spiny neurons, D1 and D2 neurons. These two neurons differ in the type of dopamine receptor they have. D1 neurons promote action, such as the act of consuming another drink, while D2 neurons halt action.
Wang’s study found that drinking large amounts of alcohol excites D1 receptors which then produce the sensation of craving. The drinker is encouraged to act and continue her drinking. Once she continues to drink, the D1 receptors are more easily activated, causing her to drink even more.
Using mice models, Wang found that the experimental, alcohol- consuming, models showed biological differences as compared to the control models. In the alcohol models, there are shown to be a greater proportion of mature medium spiny neurons with longer branching than the control group that has a greater proportion of immature, mushroom- shaped neurons. Additionally, D1 neurons are a subpopulation of neurons involved in learning and memory and Wang implicates their biological changes in the pathology of alcohol consumption.
A significant finding is that suppression of D1 neurons showed a marked decrease in the desire to drink alcohol. Stimulation of D1 neurons led to an increase in the desire to drink large amount of alcohol. Interestingly, stimulation and suppression of D2 neurons did not produce the same effect suggesting that there is a unique relationship between alcohol consumption and the D1 neuron population.
Wang reflects on his accomplishments as he says, “we’re now able to study the brain at the neuron- specific and even spine- specific level.” By identifying a subpopulation of neuroadaptational neurons that are involved in alcohol craving, Wang’s research provides many avenues for future research. These new findings, along with the many environmental and genetic factors, further add to the complexity of the “drinking” brain.
Sources:
http://news.tamhsc.edu/?post=alcoholism-a-step-toward-a-treatment
http://www.drugabuse.gov/publications/drugs-brains-behavior-science-addiction/drugs-brain
Wang J, Cheng Y, Wang X, Hellard ER, Ma T, Gil H, Ben Hamida S, and Ron D. Alcohol Elicits Functional and Structural Plasticity Selectively in Dopamine D1 Receptor-Expressing Neurons of the Dorsomedial Striatum. J. Neurosci. 2015; 35(33): 11634-11643.