We review the mechanisms by which steroid hormones masculinize two different regions of the central nervous system (CNS) in rats. Although in both cases, androgens induce a male phenotype, the detailed mechanisms are remarkably different in the two models. In the spinal nucleus of the bulbocavernosus (SNB), testosterone must be present during the perinatal period to spare motoneurons and their target muscles from cell death. This masculinization of the SNB system is through activation of androgen receptors, because XY rats with a defective gene for the androgen receptor fail to develop a masculine SNB system. Interestingly, the motoneurons are spared by androgen, even though they themselves do not possess androgen receptors during the critical period for their survival. Thus, steroids can act on one part of the body to secondarily masculinize the CNS. In the posterodorsal aspect of the medial amygdala (MePD), testosterone can induce masculine development even in adulthood, indicating that there is no critical period for steroids to affect sexual differentiation of this system. In the case of the MePD, both estrogen receptors and androgen receptors appear to mediate testosterone's masculinizing influence on neural structure. The extended neural plasticity of the MePD may reflect annual "reorganization" of the brain in the seasonally breeding ancestors of laboratory rats.