Adolescents have consistently been found to be less sensitive to many of the negative effects of alcohol [4]. For example, adolescents have decreased sensitivity to the intoxicating effects of alcohol, such as alcohol-induced sedation and motor impairment [11]. Furthermore, adolescents display reduced sensitivity to aspects of “hangover,” specifically alcohol withdrawal-induced social depression and anxiety [12,13]. Although some groups have found a reduced severity in alcohol withdrawal symptoms such as seizures [14,15], the reduced severity may be due to developmental differences in ethanol pharmacokinetics [8]. When blood alcohol concentrations are similar, withdrawal severity [16] and withdrawal-induced anxiety [17] are identical between adult and adolescent rats. However, developmental differences in alcohol's pharmacodynamic effects on GABAergic neurotransmission should also be considered. Adolescent sensitivity to alcohol sedation and/or withdrawal relies upon GABAergic neurotransmission; but, adolescent GABAA receptors are less sensitive to ethanol-induced potentiation of GABAA-mediated inhibitory currents [18]. As adverse effects of alcohol may serve as cues to halt intake or prevent future excessive intake, the adolescent's reduced sensitivity to these effects, whether pharmacodynamic or pharmacokinetic, could facilitate excessive alcohol consumption and thus increase the risk for developing an AUD [4].
