A new Penn State study found that heavy alcohol consumption in adolescents may result in permanent “dysregulation of neurons and brain cells”. These findings suggest that binge levels of alcohol exposure during adolescence, when the brain is still developing, can lead to long-lasting changes in the brain. This may set the stage for long-term behavioral changes and hint towards the mechanisms of alcohol-induced cognitive changes in humans.
Nikki Crowley, assistant professor in biology and biomedical engineering at Pennsylvania State University, explained:
“What we’re seeing here is that if adolescent binge drinking knocks neurons off this trajectory, they might not be able to get back, even if the alcohol consumption stops.”
The prefrontal cortex is an important part of the brain for tasks such as decision-making and risk assessment. According to Crowley, this area is not fully developed during adolescence and continues to mature until around age 25. Crowley notes that disruptions to its development in young people may have serious and long-lasting consequences.
“Heavy binge drinking is problematic for everyone, and should be avoided, but adolescent brains appear to be particularly vulnerable to the consequences, which in humans, will follow them for decades.”
The team, led by Avery Sicher, a doctoral student in Penn State’s neuroscience program, used a model of adolescent ethanol exposure in mice to examine how voluntary binge alcohol consumption alters different populations of neurons in the cortex, the outermost layer of the brain. In this model, mice consume alcohol in patterns that are similar to human binge drinking, which is defined by the National Institute on Alcohol Abuse and Alcoholism as a pattern of alcohol consumption that raises blood alcohol concentration to 0.08% or higher in about two hours. Binge drinking is a dangerous pattern of alcohol misuse, and understanding its impact on the developing brain can help inform treatment.
The team, led by Sicher, conducted a study on mice to investigate the effects of adolescent binge drinking on neuron circuits in the prefrontal cortex. Over the course of 30 days, mice equivalent to human ages 11-18, were given access to alcohol. The researchers then analyzed the electrophysiological properties of various neurons in the cortex to determine how the circuits were wired and fired as a result of binge drinking.
Using techniques such as optogenetics and whole-cell patch clamp electrophysiology, the team was able to isolate individual neurons and measure intrinsic excitability, including resting membrane potential and action potential firing ability. The information gathered allowed for a better understanding of how these neurons communicated with each other and how they were impacted by adolescent binge drinking.
The researchers found that somatostatin neurons, which are a key population of cells that provide inhibition of neurotransmitter release from other cell types throughout the brain and help to “dampen the noise,” appeared to be permanently dysregulated in the mice that binge drank as compared to mice that were only provided water throughout development. Somatostatin neurons release both inhibitory neurotransmitters, like GABA, as well as inhibitory peptides, like somatostatin, and proper functioning of these neurons is necessary for a healthy brain. The neurons were more excitable, meaning they were signaling too much and dampening the activity of other key neurons when the mice had transitioned into adulthood.
In-Article Image CreditsYoung male lying comatose after alcohol binge drinking via Wikimedia Commons by John Robert Smith with usage type - Creative Commons License. December 29, 2014
Featured Image CreditYoung male lying comatose after alcohol binge drinking via Wikimedia Commons by John Robert Smith with usage type - Creative Commons License. December 29, 2014