Chronic alcohol intake during adolescence, but not adulthood, promotes persistent deficits in risk-based decision making

Background: Adolescent alcohol use is a major public health concern and is strongly correlated with the development of alcohol abuse problems in adulthood. Adolescence is characterized by maturation and remodeling of brain regions implicated in decision making and therefore may be uniquely vulnerable to environmental insults such as alcohol exposure. We have previously demonstrated that voluntary alcohol consumption in adolescence results in maladaptive risk-based decision making in adulthood. However, it is unclear whether this effect on risk-based decision making can be attributed to chronic alcohol use in general or to a selective effect of alcohol use during the adolescent period.

Methods: Ethanol (EtOH) was presented to adolescent (postnatal day [PND] 30 to 49) and adult rats (PND 80 to 99) for 20 days, either 24 hours or 1 h/d, in a gel matrix consisting of distilled water, gelatin, polycose (10%), and EtOH (10%). The 24-hour time course of EtOH intake was measured and compared between adolescent and adult animals. Following 20 days of withdrawal from EtOH, we assessed risk-based decision making with a concurrent instrumental probability-discounting task. Blood EtOH concentrations (BECs) were taken from trunk blood and assessed using the Analox micro-stat GM7 in separate groups of animals at different time points.

Results: Unlike animals exposed to EtOH during adolescence, animals exposed to alcohol during adulthood did not display differences in risk preference compared to controls. Adolescent and adult rats displayed similar EtOH intake levels and patterns when given either 24- or 1-hour access per day. In addition, while both groups reached significant BEC levels, we failed to find a difference between adult and adolescent animals.

Conclusions: Here, we show that adolescent, but not adult, EtOH intake leads to a persistent increase in risk preference which cannot be attributed to differences in intake levels or BECs attained. Our findings support previous work implicating adolescence as a time period of heightened susceptibility to the long-term negative effects of alcohol exposure.