Page last updated: September 12, 2018
Study concludes, ‘excessive drinking in teens may affect short-term memory’

An animal-based study, led by Michael Salling from the Columbia University in New York and published in the journal Neuroscience, found that excessive drinking during adolescence may interfere with the activity of brain cells needed for sustaining short term memory.

According to the researchers, the prefrontal cortex (PFC) undergoes significant development during adolescence and hence may be especially susceptible to the effects of binge drinking. In humans and in animal models, adolescent alcohol exposure is known to alter PFC neuronal activity and produce deficits in PFC-dependent behaviours, such as decision making, response inhibition, and working memory.

In this study, using a voluntary intermittent access to alcohol (IA EtOH) procedure in male mice, the research demonstrated that binge-level alcohol consumption during adolescence leads to altered drinking patterns and working memory deficits in young adulthood, two outcomes that suggest medial PFC dysfunction. In addition, the study found that adolescent drinking is associated with specific changes to the intrinsic excitability of pyramidal neurons in the PFC, reducing the ability of these neurons to generate intrinsic persistent activity, a phenomenon thought to be important for working memory. These findings may help explain why human adolescent binge drinkers show performance deficits on tasks mediated by the PFC.

Teenage binge drinking is associated with reduced PFC activity, cognitive deficits, and later alcohol abuse. Yet, the mechanisms underlying these observations are unclear, the researchers said. These findings linking binge drinking with disrupted PFCdependent behaviour and brain function could ultimately lead to improved treatment of alcohol’s negative effects on the brain, they note.

Source: Alcohol consumption during adolescence in a mouse model of binge drinking alters the intrinsic excitability and function of the prefrontal cortex through a reduction in the hyperpolarization-activated cation current. Michael C. Salling, Mary Jane Skelly, Elizabeth Avegno, Samantha Regan, Tamara Zeric, Elcoma Nichols, Neil L. Harrison. The Journal of Neuroscience, 2018; 0550- 18

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