In a neurodevelopmental model of autism with age, genetic background and toxicant exposure as factors, three experiments assessed social reward in adolescent mice using an adapted social conditioned bedding preference task. Autism is a neurodevelopmental disorder behaviorally defined by restricted and repetitive activities and interests, core impairments in communication, and pervasive deficits in social interaction. Although no single causal agent has been identified, a plausible candidate may be early toxicant exposure in individuals with genetic vulnerability. The generation of reactive oxygen species may be a mechanism shared by toxicants such as valproic acid, which leads to autistic-like symptoms in both mice and humans. Thus, these experiments examined the effects of BALB/c strain, GSTM1 mice lacking an enzyme involved in oxidative stress, and BALB/c mice treated with postnatal valproic acid, on social conditioning in adolescent mice. Results revealed intact social conditioning in BALB/c mice and GSTM1 mice. However, postnatal valproic acid treatment led to social conditioning deficits and perseverative responding in adolescent BALB/c mice. Collectively, these results corroborate previous studies suggesting that early postnatal toxicant exposure induces social deficits in adolescence. Use of the social conditioning paradigm allowed assessment of deficits in individual mice, reducing potential for experimental confounds during the test. Furthermore, these experiments lay the foundation for investigations of the effects of genotype-toxicant interaction on social conditioning or subsequent social behavior.