BACKGROUND: The goal of the present study was to utilize the adolescent drug experience as an emerging vulnerability factor for developing psychiatric comorbidities in adulthood that could, in turn, help to elucidate and/or hypothesize possible mechanisms contributing to higher relapse rates. OUTCOMES: The current results showed that adolescent cocaine exposure (15 mg/kg, intraperitoneally, seven days) during early-mid adolescence (postnatal days 33-39) enhanced negative affect in adulthood, by increasing behavioral despair following drug re-exposure and by increasing anhedonia. Thus, these behavioral data provided a good model to further ascertain the long-term cellular and molecular adaptations that might take place in the brain in response to adolescent cocaine exposure as well as the impact of drug re-exposure in adulthood. In this regard, the results showed that adolescent cocaine exposure did not modulate cell proliferation (Ki-67+ cells) or c-Fos protein activation in the dentate gyrus region of the hippocampus, but attenuated c-Fos activation in the dorsal striatum. CONCLUSIONS: These results proved that a history of cocaine exposure during adolescence increased the vulnerability to induce negative affect (i.e. emergence of psychiatric comorbidity) in adulthood while it decreased neuronal activation in the dorsal striatum. Interestingly, these effects were only observed following cocaine re-exposure in adulthood, suggesting that avoiding drug contact in adulthood could prevent the long-term negative effects induced by adolescent cocaine.
BACKGROUND: The goal of the present study was to utilize the adolescent drug experience as an emerging vulnerability factor for developing psychiatric comorbidities in adulthood that could, in turn, help to elucidate and/or hypothesize possible mechanisms contributing to higher relapse rates. OUTCOMES: The current results showed that adolescent cocaine exposure (15 mg/kg, intraperitoneally, seven days) during early-mid adolescence (postnatal days 33-39) enhanced negative affect in adulthood, by increasing behavioral despair following drug re-exposure and by increasing anhedonia. Thus, these behavioral data provided a good model to further ascertain the long-term cellular and molecular adaptations that might take place in the brain in response to adolescent cocaine exposure as well as the impact of drug re-exposure in adulthood. In this regard, the results showed that adolescent cocaine exposure did not modulate cell proliferation (Ki-67+ cells) or c-Fos protein activation in the dentate gyrus region of the hippocampus, but attenuated c-Fos activation in the dorsal striatum. CONCLUSIONS: These results proved that a history of cocaine exposure during adolescence increased the vulnerability to induce negative affect (i.e. emergence of psychiatric comorbidity) in adulthood while it decreased neuronal activation in the dorsal striatum. Interestingly, these effects were only observed following cocaine re-exposure in adulthood, suggesting that avoiding drug contact in adulthood could prevent the long-term negative effects induced by adolescent cocaine.