Research suggests that adolescent binge eating causes long-term brain changes

Heavy alcohol consumption can cause permanent dysregulation in adolescent neurons, or brain cells, according to a new study in mice. The findings suggest that heavy exposure to alcohol during adolescence, when the brain is still developing, causes long-lasting changes in the brain’s ability to transmit signals and communicate. This may set the stage for long-term behavioral changes and suggests a mechanism for alcohol-induced cognitive changes in humans.

What we’re seeing here is that if adolescent binge eating and drinking knocks neurons off this trajectory, it may not be possible to get them back, even if alcohol consumption is stopped. “

Nicky Crowley, Assistant Professor of Biology and Biomedical Engineering, Hack Early Chair of Neurobiology and Neuroengineering

The prefrontal cortex is a brain region important for executive function, risk assessment, and decision making. During adolescence, the virus isn’t fully formed, Crowley said, and matures until about age 25 in humans. Impairment of that development in young people can have serious and long-term consequences, Crowley added.

“Heavy drinking is a problem for everyone and should be avoided, but the adolescent brain seems to be particularly susceptible to it, and in humans the effects will last for decades,” Crowley said. rice field.

The research team, led by Avery Shichar, a doctoral student in the neuroscience program at Pennsylvania State University, used a model of ethanol exposure during puberty in mice to show that different neuronal populations in the cortex, the outermost layer of the brain, were spontaneously activated. I understand how it changes with heavy alcohol intake. consumption. In this model, mice are known to consume alcohol in a pattern similar to that of humans. It is defined by the National Institute of Alcohol Abuse and Alcoholism as an alcohol consumption pattern that results in a blood alcohol concentration of 0.08% or more, usually in about 2 hours. Binge eating is considered one of the most dangerous patterns of alcohol misuse, and understanding its effects on the developing brain can help inform treatment.

Sicher et al. gave mice alcohol for 30 days. Due to their rapid development and short lifespan, this corresponds to approximately 11-18 years of age in humans. They then examined the electrophysiological properties of various neurons throughout the prefrontal cortex to understand how adolescent binge eating affects the wiring and firing of these circuits. Sitcher et al. The research team used whole-cell patch-clamp electrophysiology combined with techniques such as optogenetics, which allowed the team to isolate individual neurons and analyze their unique properties, such as the resting membrane potential and each neuron’s ability to fire action potentials. We were able to record measures related to the excitability of This allowed us to understand how these neurons changed their ability to send signals to other neurons.

They found that somatostatin neurons, a key cell population that inhibits the release of neurotransmitters from other cell types throughout the brain and helps ‘silence out the noise’, were more active in gluttonous mice than in gluttonous mice. appeared to be permanently dysregulated in comparison. Only water was provided during development. Somatostatin neurons release both inhibitory neurotransmitters such as GABA and inhibitory peptides such as somatostatin. Proper functioning of these neurons is necessary for a healthy brain. Neurons became more excitable – meaning there was too much signal and less activity in other key neurons -; 30 days after the mice had stopped drinking, the mice reached adulthood. when migrated.

“Neurons have a relatively fixed developmental trajectory. To function properly, they need to reach their destination and synchronize with the right partner during specific periods of development,” Crowley explains. Did.

David Stearns, a biology student at Schleyers Honor College, measured somatostatin cell numbers to quantify cell density before and after ethanol intake. He found that the number of SST neurons did not appear to change as a result of binge eating, although electrophysiology data suggested that these neurons were wired differently.

Other authors on this paper include Keith Griffiths, a research technician in the lab and a former undergraduate student in engineering sciences and mechanics; Grace Smith, a graduate student in biomedical engineering; and a graduate student in neuroscience. Dakota Brockway, and former researcher Nigel Dao. Lab Technician and current PhD student at New York University. This research was supported by the Pennsylvania State Institute of Health and the Huck Institute for Life Sciences.

If you want to learn more about Schicher’s neuroscience research, check this out. short video From Hack Institute’s Student Spotlight series. The paper is now available online in the journal Neuropharmacology and will be published in the August 15th issue.