Dentate granule cells are enriched with receptors for the stress hormone corticosterone, i.e., the high-affinity mineralocorticoid receptor (MR), which is already extensively occupied with low levels of the hormone, and the glucocorticoid receptor (GR), which is particularly activated after stress. More than any other cell type in the brain studied so far, dentate granule cells require hormone levels to be within the physiological range. In the absence of corticosteroids, proliferation and apoptotic cell death are dramatically enhanced. Dendritic morphology and synaptic transmission are compromised. Conversely, prolonged exposure of animals to a high level of corticosterone suppresses neurogenesis and presumably makes dentate granule cells more vulnerable to delayed cell death. These corticosteroid effects on dentate cell and network function are translated into behavioral consequences, in health and disease.