|Whether exposure to methylmercury (MeHg), an environmental neurotoxicant, during adolescence alters the brain and behavior is only beginning to be explored. The continued maturation of mechanisms that control neuronal gene expression, such as DNA methylation and histone modifications, may predispose the adolescent brain and behavior to be particularly susceptible to MeHg exposure. In Experiment 1, male C57BL6/n mice were exposed to 0, 0.3, and 3.0 ppm MeHg (n = 12 each) via drinking water from postnatal days 21 to 60 (murine adolescence). As adults, mice were trained to lever press under an ascending series of fixed-ratio schedules of milk reinforcement. Adolescent MeHg exposure dose-dependently decreased estimates of response-reinforcer coupling and minimum response time relative to controls. Further, adolescent MeHg increased maximum response rates in exposed mice relative to controls. In Experiment 2, the protective effects of sodium butyrate (NaB; a histone deacetylase inhibitor) and environmental enrichment on MeHg-induced behavioral impairment were examined. Male C57BL6/n mice were assigned to control, NaB, or environmental enrichment and within each of these treatment conditions were given either 0 or 3.0 ppm MeHg. Adolescent MeHg exposure again decreased estimates of response-reinforcer coupling but did not significantly alter minimum response time. Chronic NaB also decreased response-reinforcer coupling. These data suggest that behavioral mechanisms of adolescent MeHg exposure may be related to motoric capacity and the impact of reinforcement on prior responses.