Steroids stimulate male sexual behavior through interconnected limbic nuclei, including the medial amygdala (Me) and medial preoptic area (MPOA). Although Me and MPOA each can transduce hormonal cues to induce sexual activity in castrated male hamsters, simultaneous stimulation of Me and MPOA fails to amplify mating. The present study extends our investigations of redundancy in the hormonal control of mating by testing the behavioral effects of (1) increasing steroid dose in a single brain region or (2) locally blocking steroid action with an estrogen antagonist. In Experiment 1, sexually experienced castrates received a single testosterone implant in Me, bilateral testosterone implants, or a single implant of a highly potent androgen, 7a-methyl-19-nortestosterone (MENT). These treatments stimulated mating behavior: 2 weeks after surgery, mounting was observed in > or =50% of the males in each group. In Experiment 2, castrated males received intracerebral implants of the estrogen antagonist tamoxifen in Me or MPOA, combined with systemic testosterone replacement. Tamoxifen in MPOA had minimal effects on the recovery of mating behavior. With tamoxifen in Me, mounts and intromissions were significantly reduced 18 days after surgery. However, the percent of males in each group that expressed mounts, intromissions or ejaculations was not different. Thus, in Experiment 1, increasing the amount of steroid does not amplify mating. Likewise, local blockade of hormone action in Experiment 2 does not prevent behavior. These findings support the concept that steroids are largely permissive for male sex behavior. Steroid stimulation of either Me or MPOA is sufficient for sexual activity. Conversely, neither Me nor MPOA has an absolute requirement for hormones to facilitate expression of mating.