Among antidepressant treatments, electroconvulsive therapy (ECT) is the most efficacious treatment for depression, but the cellular mechanisms underlying the actions of ECT are unknown. Electroconvulsive stimulation (ECS), an animal model of ECT, robustly stimulates hippocampal neurons and gene transcription and enhances adult neurogenesis in the dentate gyrus (DG) of hippocampus. In this study, we focused on CREB, a transcription factor expressed in the hippocampal DG and activated by signals in response to extracellular stimuli. To clarify the role of CREB on increased neurogenesis and expression change in the DG by chronic ECS, we generated adeno associated virus (AAV) expressing GFP and artificial microRNA targeting CREB (miR-CREB) and injected it into the mouse DG. Knockdown (KD) of CREB expression in the DG was confirmed by immunostaining 5 weeks after AAV injection. Eleven times of ECS were administered to CREB KD animals and immunostaining was performed. The repeated ECS significantly increased the number of NeuroD1-positive neural progenitor cells and doubulecortin-positive immature neurons and their dendric elongation in control mice. We found that these cellular changes by repeated ECS were attenuated in the DG of CREB KD animals. We will continue to elucidate whether CREB is involved in these ECS-induced changes in gene expression and whether they correspond to histological changes.