The developmental period from adolescence to adulthood is accompanied by a greater vulnerability to addictions -- including alcohol use disorders -- than is seen in other periods of life. This increased risk may be due to genetic predisposition, poor impulse control, or heightened sensitivity of the still-developing brain to drug-related toxicity. This report describes a study in mice of the neurobehavioral impact of chronic, intermittent alcohol-vapor exposure during adolescence, in an effort to model periodic heavy drinking and compare it with similar drinking behavior during adulthood. Researchers conducted two parallel tests in adult male mice following their exposure to alcohol vapors during adolescence (4-6 weeks old) or adulthood (8-10 weeks old). First, they tested the adult mice for changes in the density and structure of dendritic spines (nerve endings) in the infralimbic cortex (IL), prelimbic cortex (PL) and basolateral amygdala (BLA) regions of the brain. Second, they tested the adult mice for alcohol drinking, sensitivity to alcohol intoxication, blood-alcohol clearance, and measures of response to food reward. Chronic exposure to alcohol vapors during adolescence produced significant, persistent, and strong regional-specific alterations in neuronal dendritic spine density in IL and BLA neurons, accompanied by a limited set of behavioral alterations. Comparable effects were not seen in the mice exposed to alcohol only during adulthood. Together, these data demonstrate that specific key brain circuits are vulnerable to alcohol's effects during adolescence, with lasting and potentially detrimental consequences for behavior. Source
