Structural neuronal network plasticity is associated with epileptogenesis during limbic kindling, but the full extent of network changes is not well understood. We investigated whether dentate granule cell (DGC) neurogenesis, which continues into adulthood in the rodent, is altered in the amygdala kindling model of epileptogenesis. Adult rats were stimulated to either 4-6, 9-10 or 19-20 class 4/5 (generalized) kindled seizures. 5-Bromo-2'-deoxyuridine labeling showed that cell proliferation increased in the dentate gyrus only in animals that experienced nine or more class 4/5 kindled seizures. Immunocytochemistry for neuronal markers revealed that many of the newly generated cells differentiated into DGCs in the inner aspect of the DGC layer. The lack of increased DGC neurogenesis after fewer kindled seizures or at early timepoints following kindling suggests that this process is not involved in kindling development. Instead, newly generated DGCs may be important for maintenance of the kindled state or the increased susceptibility to spontaneous recurrent seizures.