Epileptiform activity (EA) is comprised of abnormal excessive neuronal discharges (spikes and sharp waves) that can be detected in the electroencephalogram. Although originally associated with epilepsy, EA is also present in many other conditions such as Alzheimer’s disease, Parkinson’s disease, Autism Spectrum Disorder, dementia, traumatic brain injury and aging. Increasing evidence suggests that EA may contribute to the cognitive impairments seen in these conditions, including deficits in memory, learning, decision-making, and mood regulation. The precise neurobiological mechanisms linking EA to these behavioral deficits remain unclear; however, adult hippocampal neurogenesis has emerged as a potential underlaying mechanism. Using a pure model in which EA is induced without causing seizures, we investigated structural and functional changes on hippocampal immature neurons born at the time of the induction of EA or born 2 months after the induction. EA induced morphological alterations in newborn neurons such as abnormal migration and more complex dendritic arborization in increased density of dendritic spines. To address whether these morphological changes translate into functional alterations we are currently performing whole-cell patch-clamp recordings on retroviral vector-labeled newborn neurons. Our data show that EA induces functional alterations in newborn neurons born 2 months after the induction of EA.