Comparison of the deleterious effects of binge drinking‐like alcohol exposure in adolescent and adult mice

Abstract

A major cause of alcohol toxicity is the production of reactive oxygen species generated during ethanol metabolism. The aim of this study was to compare the effect of binge drinkinglike alcohol exposure on a panel of genes implicated in oxidative mechanisms in adolescent and adult mice. In adolescent animals, alcohol decreased the expression of genes involved in the repair and protection of oxidative DNA damage such as atr, gpx7, or nudt15 and increased the expression of proapoptotic genes such as casp3. In contrast, in the adult brain, genes activated by alcohol were mainly associated with protective mechanisms that prevent cells from oxidative damage. Whatever the age, iterative binge-like episodes provoked the same deleterious effects as those observed after a single binge episode. In adolescent mice, multiple binge ethanol exposure substantially reduced neurogenesis in the dentate gyrus and impaired short-term memory in the novel object and passive avoidance tests. Taken together, our results indicate that alcohol causes deleterious effects in the adolescent brain which are distinct from those observed in adults. These data contribute to explain the greater sensitivity of the adolescent brain to alcohol toxicity.

Differential Sensitivity to Ethanol‐Induced Circadian Rhythm Disruption in Adolescent and Adult Mice

“…Second, we did not measure blood ethanol concentrations (BEC) in the present study. However, two other studies failed to detect age-related differences in ethanol clearance in this strain at 20–30 min after ethanol administration (the interval between injection and the light pulse in our study; (Hefner and Holmes, 2007, Linsenbardt et al, 2009), while a third study reported no age difference in BEC at all (Lacaille et al, 2015). A third limitation is that only photic phase-delays were examined in this report, because adult mice typically show only small advances to light.…”

“…During adolescence, mice of this strain consume more alcohol than adults, particularly in models of limited access, intermittent access, and binge-drinking (Holstein et al, 2011, Melendez, 2011, Moore et al, 2010, Quoilin and Boehm, 2016; but see also Hefner and Holmes, 2007). Adolescent C57BL/6J mice also show differential sensitivity to acute ethanol, including increased sensitivity to ethanol-induced locomotor stimulation (Hefner and Holmes, 2007, Melon and Boehm, 2011), anxiolysis (Hefner and Holmes, 2007), and certain memory impairments (Lacaille et al, 2015, Spanos et al, 2012), and decreased sensitivity to ethanol-induced conditioned taste aversion (CTA; (Holstein et al, 2011, Moore et al, 2013), sedation (Hefner and Holmes, 2007, Linsenbardt et al, 2009), hypothermia and locomotor suppression (Lopez et al, 2003). …”

Cognitive and neurobehavioral benefits of an enriched environment on young adult mice after chronic ethanol consumption during adolescence

“…Moreover, BD effects are correlated with cognitive damage in young people as abusive EtOH consumption can have deleterious effects on the adolescent brain (Lacaille et al . ). It causes a significant loss of hippocampal neurons, astrocytes and microglia (Oliveira et al .…”

Viral-mediated overexpression of the Myelin Transcription Factor 1 (MyT1) in the dentate gyrus attenuates anxiety- and ethanol-related behaviors in rats

“…Also, results have demonstrated that chronic antidepressant treatment significantly increased neuronal proliferation in the adult DG (Malberg et al 2000), and anxiety induced by stress and depression-like conditions in animal models are associated with reduced DG proliferation (Czeh et al 2001). Furthermore, multiple binge ethanol exposure substantially reduced neurogenesis in the DG of adolescent mice (Lacaille et al 2015). Also, moderate alcohol consumption reduced the number of cells produced in the DG by nearly 40% (Anderson et al 2012).…”