Limited access ethanol drinking in the dark in adolescent and adult mice

Portland Alcohol Research Center, Research Service, VA Medical Center, OR 97239, USA.
Pharmacology Biochemistry and Behavior (Impact Factor: 2.78). 04/2011; 98(2):279-85. DOI: 10.1016/j.pbb.2011.01.003
Source: PubMed


Adult risk of alcohol dependence increases the younger one first engages in intoxicating consumption. Adolescent mice drink more ethanol than do adults on a gram per kilogram basis, an increase sometimes persisting into adulthood, and this is genotype-dependent. Most studies have used 24 h two-bottle preference, with a choice between ethanol and water. We studied the developmental onset of binge drinking using limited access ethanol drinking in the dark (DID) in male and female mice. To establish age dependence in DID magnitude, we tested HS/Npt mice of 6 ages for DID for 2 weeks, and when they were 9 weeks old, we retested them for 2 weeks vs naïve adult controls. Age groups drank equivalently in their first week; thus, adolescent HS/Npt mice do not show greater DID than adults. Six week old mice drank more ethanol during their second week relative to their other weeks. Ethanol DID during early adolescence (4 weeks) led to increased drinking in adulthood, as did initial DID exposure at 8 weeks. High drinking in the dark-1 (HDID-1) mice (4, 6, 9 weeks old), selectively bred for high blood ethanol after DID, were tested for 9 weeks. Mice beginning at 4 weeks generally drank more ethanol than those of other age groups. Comparison at the same ages showed that 9 week olds initiated at 4 weeks drank more ethanol than did naïve 9 week olds, but all three groups of age-matched mice drank equivalent amounts once they were 10 weeks and older. The DID test is thus sensitive to developmental age. DID intakes by young adolescent HDID-1 mice were greater than intakes by older mice, like those shown by studies with two-bottle preference. Early DID led to increased drinking as adults only in HS/Npt mice. HDID-1 mice provide a useful animal model for exploring whether DID and continuous access preference drinking have parallel consequences when initiated in adolescence.

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    • "This increase was associated with a positive modulation of ERK2 signaling in the striatum. The effects of early ethanol exposure on ethanol consumption at adulthood (Molet et al., 2012) and central DA neurotransmission, well known to be implicated in the rewarding effects of drugs of abuse (Di Chiara and Imperato, 1988), gave rise to numerous studies for the last years (Badanich et al., 2007; Guerri and Pascual, 2010; Metten et al., 2011). However, whether such an early exposure could affect the perception of the rewarding properties of these drugs at adulthood was not yet investigated. "
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    • "For example, ethanol drinking at adulthood has been shown to be either promoted (Hargreaves et al., 2009; Maldonado-Devincci et al., 2010) or unaffected (Vetter et al., 2007) by ethanol administration in adolescent rats. In mice, data are also rather inconsistent (Blizard et al., 2004; Ho et al., 1989; Metten et al., 2011), suggesting that the effects of early ethanol exposure on adult drinking depend on several factors such as ethanol intake conditions, the age and the strains of the rodents exposed to ethanol. "
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    • "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. "
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