The function of the N-terminal domain of steroid hormone receptors is not fully understood, and appears to modulate transcription. Antibodies to steroid hormone receptors are generally directed against the N-terminal region because of its strong hydrophilicity. Estrogen receptor immunoreactivity was localized in the nuclei of neurons, not in the cytoplasm or non-neuronal cells (glia, endothelium, and ependymal cells) in the ovariectomized rat. The medial preoptic area of female rat contains more neurons containing the estrogen receptor immunoreactivity than male. In the anteroventral periventricular nucleus of the preoptic area (AVPN-POA), estrogen receptor immunoreactive neurons are present in numbers several times higher in females than males. Estrogen treatment of ovariectomized rats reduces the number of estrogen receptor-immunoreactive neurons in the AVPN-POA of females. It was found that neurons extending their axons and dendrites contain estrogen receptors. Whether axons or dendrites are specifically affected by gonadal steroids is still controversial, because hypothalamic neurons have no distinctive polarity such as neurons in the hippocampus. The number of cells containing glucocorticoid receptor immunoreactivity and the intensity of immunoreactivity per cell showed age-related variations. Immunohistochemical studies using an antibody against rat liver glucocorticoid receptor showed that overall intensity of glucocorticoid receptor immunoreactivity in the brain was the highest perinatally, decreased to a low intensity around postnatal day 12, and thereafter increased gradually again to moderate staining in most brain areas. Dexamethasone treatment at the neonatal period induces apoptotic changes of granule cells in the dentate gyrus. This suggests that adrenal steroids have an indirect influence on cell birth through an as yet unidentified mechanism.