“Binge” drinking experience in adolescent mice shows sex differences and elevated ethanol intake in adulthood

Abstract

Binge drinking, defined as achieving blood ethanol concentrations (BEC) of 80 mg%, has been increasing in adolescents and was reported to predispose later physical dependence. The present experiments utilized an animal model of binge drinking to compare the effect of ethanol “binge” experience during adolescence or adulthood on subsequent ethanol intake in male and female C57BL/6 mice. Adolescent and adult mice were initially exposed to the scheduled high alcohol consumption procedure, which produces BECs that exceed the levels for binge drinking following a 30 min ethanol session every third day. Ethanol intake and BECs were significantly higher in the adolescent (∼3 g/kg, 199 mg%) versus adult (∼2 g/kg, 135 mg%) mice during the first three ethanol sessions, but were more equivalent during the final two ethanol sessions (1.85-2.0 g/kg, 129-143 mg%). Then, separate groups of the ethanol experienced mice were tested with ethanol naïve adolescent and adult mice for 2-hr limited access (10 and 20% solutions) or 24-hr (5, 10 and 20% solutions) ethanol preference drinking. Limited access ethanol intake was significantly higher in female versus male mice, but was not altered by age or ethanol experience. In contrast, 24-hr ethanol intake was significantly higher in the adolescent versus adult mice and in female versus male mice. Furthermore, binge drinking experience in the adolescent mice significantly increased subsequent ethanol intake, primarily due to intake in female mice. Thus, adolescent binge drinking significantly increased unlimited ethanol intake during adulthood, with female mice more susceptible to this effect.

Reinforcing Properties and Neurochemical Response of Ethanol within the Posterior Ventral Tegmental Area Are Enhanced in Adulthood by Periadolescent Ethanol Consumption

“…In contrast, adolescents injected with EtOH in a manner that does not produce taste aversion can enhance adult EtOH consumption (Pascual et al, 2007(Pascual et al, , 2009Maldonado-Devincci et al, 2010). Voluntary EtOH drinking during adolescence at a level that produces pharmacologically relevant levels of EtOH has been shown to enhance adult EtOH consumption (Walker and Ehlers, 2009;Strong et al, 2010;O'Tousa et al, 2013). In P rats, adolescent EtOH consumption (oral freechoice) increases the acquisition of EtOH self-administration (operant), decreases the rate of extinction of EtOH selfadministration, enhances relapse drinking, and enhances the ability of a priming dose of EtOH to increase EtOH-seeking (Rodd-Henricks et al, 2002a).…”

Advancing Addiction Treatment: What Can We Learn from Animal Studies?

“…Recent data also demonstrate that limited access to alcohol during adolescence causes increased baseline (Metten et al 2011;Strong et al 2010) and dependence-related alcohol consumption in adulthood (Gilpin et al 2012). Thus, limitedaccess adolescent drinking paradigms appear to be successful in modeling both the binge-like pattern of adolescent drinking behavior and the consequences of adolescent alcohol consumption on adult alcohol use and risk of dependence.…”

“…For example, investigators have studied adolescent rats and mice that voluntarily drink more than adults under both continuous-access (Doremus et al 2005;Tolliver and Samson 1991;Truxell et al 2007;Vetter et al 2007) and limited-access conditions (Maldonado-Devincci et al 2010;Metten et al 2011). In addition, some adolescent rodents actually do drink to intoxication, especially when tested in limited-access paradigms (Rhodes et al 2005;Strong et al 2010).…”

Translational Models of Interactions Between Stress and Alcohol Consumption: Strengths and Limitations

“…There are a number of rodent models for binge drinking, including limited access in operant conditions in rats (Simms et al 2010), excessive drinking in dependent rats and mice (Griffi n et al 2009;Richardson et al 2008;Sommer et al 2008), and, in mice, "drinking in the dark" 1 (Sparta et al 2008) and scheduled high access models (Strong et al 2010), in which limited access promotes excessive alcohol intake. These studies have identifi ed a number of molecular regulators of binge intake, including stress-related molecules (discussed below).…”