Overall, the expression level of miR-182-5p was upregulated in the hippocampus of CSDS-induced mice, and administration of AAV-siR-182-5p ameliorated depression-like behaviors and defective neurogenesis in CSDS-induced mice, which seemed to be facilitated via activation of the hippocampal Akt/GSK3β/CREB signaling pathway. This evidence concerns the gene AKT1 and depressive symptom measurement.