Besides motor ataxia, anxiety has been shown to play a role in the recurrence and initiation of drinking behavior. Given the role of the GABAA receptor system in anxiety, it is reasonable to surmise that the adolescent developmental period may be characterized by changes in the anxiolytic effects of ethanol. Recent studies report attenuated withdrawal-related anxiety and a lessened anxiolytic effect of ethanol in adolescent rats as measured in a social interaction test (Doremus et al. 2003; Varlinskaya and Spear 2002, 2004). Interestingly, early adolescent C57BL/6J mice show enhanced anxiety and greater anxiolytic response to ethanol on the elevated plus maze (Hefner and Holmes 2007). In addition to potential species differences, such contrary results are also likely confounded by different baseline levels of social interaction and plus maze behavior between adolescence and adults. However, it is possible that lessened anxiogenesis and increased anxiolysis during adolescence may also be a reflection of the developmental state of the GABAA receptor system that underlies anxiety and may be a contributing factor to problem drinking. Salimov et al. (1996) reported that ethanol consumption during
