In Experiment I, castrated male and female CD-1 mice +/- estradiol benzoate (EB) treatment were tested for their performance on a skilled sensorimotor task consisting of walking across beams of varying widths (6, 9, 12, and 21 mm). To evaluate whether behavioral performance was related to nigrostriatal dopaminergic function, tissue dopamine concentrations were determined from the corpus striatum as well as the hypothalamus and olfactory tubercle. In general, sensorimotor performance improved for all treatment conditions as the beam width increased. Castrated male mice treated with oil vehicle showed the worst performance as indicated by significantly greater amounts of time to cross the beam. Treatment of castrated males with EB significantly improved their performance. Performance of the castrated females was not changed by EB treatment and was similar to that observed with the castrated + EB males. Significant gender differences in dopamine concentrations (female > male) were obtained in the corpus striatum, as well as the olfactory tubercle and hypothalamus. Dopamine levels were unaltered by EB treatment. In Experiment II, behavioral and neurochemical determinations were directly compared between castrated and intact male mice. Behavioral performance of castrates was significantly reduced compared to intact males. No differences in dopamine concentrations were obtained between these two groups; however, the hypothalamic dopamine/DOPAC ratio of castrates was significantly greater than that of intact male mice. These results demonstrate significant modulatory effects of EB in castrated male, but not female, mice upon sensorimotor performance and indicate that this task may provide an effective means to partial out modulatory effects of gonadal steroid hormones upon skilled sensorimotor performance. When the data of Experiments I and II are combined, it appears that the basis of this sensorimotor deficit in the males is the absence of gonadal steroid hormones. In addition, these results reveal significant gender differences in various dopaminergic systems in these mice. (C) 1994 Academic Press, Inc.