Kindling, a form of neuronal plasticity produced by repeated low intensity electrical brain stimulation, leads to epileptic seizures. To address possible causes of this phenomenon, we have prepared amygdala-kindled animals and measured neurogenesis, by bromodeoxyuridine incorporation. Early, when focal seizures were present, there was no evidence of a change in the rate of hippocampal neurogenesis. In contrast, during the later phases of kindling, when secondary generalization was well established and motor seizures were present, neurogenesis was enhanced by 75-140%, depending on the hippocampal region. Double labelling with the neuron-specific marker TOAD-64 demonstrated the presence of numerous new-born granule neurons in the kindled animals. We propose that the newly-born neurons contribute to the cellular changes and behavioral symptoms associated with this type of epileptiform brain plasticity.