Excessive alcohol consumption in adolescence can cause lasting changes to neurons in the brain, as demonstrated by a new study in mice. These changes can impair the brain’s ability to signal and communicate, leading to long-term behavioral changes. The prefrontal cortex, responsible for executive functioning, decision making, and risk assessment, is particularly vulnerable during adolescence as it is still developing until around age 25. Somatostatin neurons, which provide inhibition of neurotransmitter release from other cells, were found to be permanently dysregulated in mice that drank excessively compared to those that did not. These neurons were more excitable, signaling too much and dampening the activity of other key neurons. The study suggests that understanding the impact of binge drinking on the developing brain can inform treatment, as heavy drinking is one of the most dangerous patterns of alcohol abuse.
Additional Piece:
Alcohol consumption among adolescents has become a prevalent issue in today’s society, leading to concerns about the long-term impact on their health and well-being. The new study provides insight into how such excessive drinking can cause lasting changes in the brain, particularly in the prefrontal cortex, which is responsible for many important functions, including decision making. These findings should be seen as a call to action to prevent alcohol consumption among youth, as the consequences can follow them for decades.
One of the most critical takeaways from this study is that adolescent brains appear to be particularly vulnerable to the consequences of excessive drinking. This vulnerability can lead to long-term, permanent changes in the developing brain’s ability to signal and communicate, which can cause behavioral changes that can have serious ramifications for the individual’s future. Parents, educators, physicians, and other stakeholders must work together to create awareness and provide support, guidance, and education to youth about the dangers of alcohol consumption.
The study’s findings demonstrate that early intervention can help prevent the onset of alcohol abuse, particularly among vulnerable adolescents. It is essential to educate youth about the dangers of alcohol consumption and promote responsible behavior, as well as provide access to appropriate resources and support for those who may be struggling with addiction. As a society, we must come together to prioritize the health and well-being of our youth and create a culture that supports responsible drinking behavior.
In addition to awareness and education, it is essential to provide resources and support for those who may be struggling with addiction. This support can include counseling, therapy, and treatment programs that specialize in addiction recovery. Education and awareness campaigns should emphasize the importance of seeking help if needed and normalize the process of seeking treatment.
Overall, the study highlights the dangers of excessive alcohol consumption in adolescence and emphasizes the need for increased awareness, education, and support for youth. By working together, we can create a culture that prioritizes responsible drinking behavior and provides resources and support for those who may need it. It is our responsibility as a society to ensure the health and well-being of our youth and promote healthy lifestyles and behaviors that will set them up for success in the future.
Summary:
A new study shows that excessive alcohol consumption can cause lasting changes in the developing brain, particularly in the prefrontal cortex, which may have long-term behavioral consequences. The study used a mouse model of adolescent ethanol exposure and found that somatostatin neurons, which inhibit neurotransmitter release from other cells, were permanently dysregulated in mice that drank excessively compared to mice that did not. The findings emphasize the need for increased awareness, education, and support for youth to promote responsible drinking behavior and provide access to appropriate resources and support for those who may be struggling with addiction.
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Excessive alcohol consumption may cause permanent dysregulation of neurons, or brain cells, in adolescents, according to a new study in mice. The findings suggest that exposure to binge levels of alcohol during adolescence, when the brain is still developing, leads to lasting changes in the brain’s ability to signal and communicate, which could set the stage for long-term behavioral changes. term and hint at the mechanisms of alcohol-induced cognitive changes in humans.
“What we’re seeing here,” said Nikki Crowley, assistant professor of biology and biomedical engineering and chair of the Huck Early Chair in Neurobiology and Neural Engineering, “is that if adolescents drink to excess they throw neurons off this trajectory, it’s they may not be able to get even if alcohol use stops.
The prefrontal cortex is a key brain region for executive functioning, risk assessment, and decision making. According to Crowley, it is not fully formed in adolescents and is still maturing in humans until around age 25. Interruptions in their development in the young can have serious and long-lasting consequences, Crowley added.
“Excessive alcohol consumption 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,” Crowley said.
The team, led by Avery Sicher, a doctoral student in Penn State’s neuroscience program, used a mouse model of adolescent ethanol exposure to understand how different populations of neurons in the cortex, the outermost layer of the brain, they are modified by voluntary alcohol binges. consumption. In this model, mice are known to consume alcohol in patterns that approximate human binge drinking, defined by the National Institute on Alcohol Abuse and Alcoholism as a pattern of drinking that leads to a concentration of alcohol in the blood of 0.08% or more, usually in about two hours. Heavy drinking is considered one of the most dangerous patterns of alcohol abuse, and understanding its impact on the developing brain can help inform treatment.
Sicher and his colleagues gave the mice access to alcohol for a period of 30 days. Due to their faster development and shorter lifespan, this corresponded to roughly 11 to 18 years in human years. They then looked at the electrophysiological properties of different neurons throughout the prefrontal cortex to understand how adolescent binge drinking influenced the wiring and activation of these circuits. Sicher et al. used whole-cell patch-clamp electrophysiology, combined with techniques such as optogenetics, which allowed the team to isolate individual neurons and record measurements related to intrinsic excitability, such as resting membrane potential and the ability of each neuron to fire potentials. action. This allowed them to understand how these neurons had changed their ability to signal with other neurons.
They found that somatostatin neurons, a key population of cells that provide inhibition of neurotransmitter release from other cell types throughout the brain and help “muffle noise,” appeared to be permanently dysregulated in the mice that drank to excess in compared to mice that were only provided with water throughout development. Somatostatin neurons release inhibitory neurotransmitters, such as GABA, as well as inhibitory peptides such as somatostatin, and proper function 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, until 30 days after the mice stopped drinking alcohol, when the mice transitioned into adulthood.
“Neurons have a relatively fixed developmental trajectory: They need to get where they’re going and synchronize with the right partners during specific periods of development to function properly,” Crowley explained.
David Starnes, an undergraduate biology student at Schreyer’s Honor College, performed somatostatin cell counts to quantify cell density before and after ethanol consumption. He found that while electrophysiological data suggested that these neurons wire differently, the number of SST neurons does not appear to change as a result of excessive alcohol consumption.
Other authors on the paper include Keith Griffith, a research technician in the lab and former BS in Engineering Sciences and Mechanics, Grace Smith, a graduate student in Biomedical Engineering, Dakota Brockway, a graduate student in neuroscience, and Nigel Dao, a former laboratory technician researcher and current doctoral student at New York University. This research was supported by the National Institutes of Health and the Huck Institutes of Life Sciences at Penn State.
https://www.sciencedaily.com/releases/2023/06/230609123038.htm
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