Different from neurogenesis that occurs under physiological conditions, enhanced neurogenesis in the dentate gyms of the hippocampus following seizure activity, especially status epilepticus (SE), is associated with ectopic residence and aberrant integration of newborn granule cells.Hilar ectopic granule cells are considered to be detrimental to the stability of dentate circuitry mainly because of their altered morphologies, special intrinsic electrophysiological properties and synaptic connectivity.We hypothesized that SE also increases ectopic granule cells in the molecular layer and those newly generated granule cells located in the molecular layer are different from those normally located granule cells both morphologically and electrophysiologically.SE in male SpragueDawley rats was induced by intraperitoneal injection of pilocarpine.We verified the presence of abnormally migrated newborn granule cells in the molecular layer by doublecortin (DCX) immunostaining days after the induction of SE and quantified mature granule cells in the molecular layer by double labeling of prospero homeobox protein 1 (Prox 1) and neuron-specific nuclear protein (NeuN) months later.DCX immunostaining showed that different to the distribution pattern of DCX-positive cells in control rats, many DCX-positive cells were present in the molecular layer 7 days after the induction of SE with abnormal polarization.At least 10 weeks after SE, the estimated number of cells positive for both Prox 1 and NeuN in the molecular layer nearly doubled.In electrophysiological aspects, ectopic granule cells in the molecular layer following SE were more heterogeneous than those normally located granule cells.We conclude that following SE, aberrant neurogenesis occurs in the molecular layer and those molecular layer-located granule cells generated after SE are different from normally located granule cells morphologically and electrophysiologically.