Abstract Neurogenesis persists in the olfactory bulbs of adult mice, with new cells being generated in the proliferative subependymal layer. Our previous work has shown that unilateral odor deprivation through naris closure leads to a net loss of granule neurons in the ipsilateral (odor-deprived) olfactory bulb, while not affecting the contralateral bulb. Here we used several experimental approaches to determine if this loss of neurons results from reduced neurogenesis, reduced neuronal survival, or both. First, bromodeoxyuridine immunohistochemistry was used to determine the number of S-phase cells in the subependymal layer eight weeks after naris closure. Proliferation was reduced within and just caudal to the odor-deprived bulb compared to the open-side (control) bulb. Second, counts of pyknotic nuclei four weeks after naris closure were used to document a higher rate of cell death on the deprived side. Third, 3H-thymidine autoradiography was used to assess differences in granule cell survival on the two sides. Granule cell precursors were labeled by a single injection of 3H-thymidine eight weeks after naris closure, and the number of surviving labeled granule cells assessed four and 16 weeks later. Granule cell survival was significantly reduced within the odor-deprived bulbs. These data indicate that the loss of granule cells which follows odor deprivation is caused, at least in part, by reduced neurogenesis and reduced survival of these adult-generated neurons.