Adolescent drinking targets corticotropin-releasing factor peptide-labeled cells in the central amygdala of male and female rats.

Adolescence is a developmental period when many teenagers first drink alcohol and often engage in binge drinking. Early onset of alcohol is linked to increased risk of stress-related disorders in adulthood in humans, suggesting that alcohol may interfere with development of the stress regulatory system. We investigated the effect of voluntary alcohol exposure on corticotropin-releasing factor (CRF) peptide-producing cells in the central nucleus of the amygdala (CeA) in adolescent male and female rats. These cells are important for the autonomic and behavioral responses to stress, have been implicated in addiction, and change over adolescent development. Animals self-administered sweetened alcohol during early adolescence (postnatal days (PDs) 28-42) and brains were obtained on PD 43 for CRF peptide immunolabeling. Females had fewer CRF immunoreactive (-ir) cells in the CeA compared to males. In both males and females, alcohol self-administration reduced the number of CRF-ir cells in the CeA compared to control conditions in which rats self-administered equivalent levels of sweetened water that did not contain alcohol. Reduced peptide labeling was not observed in the bed nucleus of the stria terminalis, indicating regional specificity of these changes. Alterations within the CRF cell population of the amygdala may have important implications for susceptibility to alcohol and stress disorders during adolescence and later on in life.