ASIC1a (acid-sensing ion channel-1a) is a neuronal acid-activated cation channel located in the postsynaptic membrane. The channel receives synaptic protons, contributing to synaptic plasticity, learning and memory. It is well known that adult neurogenesis is enhanced after ischemic brain injury accompanied with local tissue acidosis. However, the relationship between adult neurogenesis and ASIC1a remains to be elucidated. We investigated whether ASIC1a is expressed in newborn dentate granule cells (DGCs) in the adult mouse brain. Patch-clamp experiments in whole-cell mode recorded proton-induced ASIC1a-like currents in newborn DGCs examined. To examine the potential roles of ASIC1a in mouse adult hippocampal neurogenesis, we used an onco-retrovirus-mediated approach to genetically label and manipulate newborn DGCs in vivo. Three-dimensional reconstruction of confocal Z-stucks generated by IMARIS software was applied to morphologically characterize the dendritic arborization and spine formation of ASIC1a-deficient newborn DGCs labeled with EGFP. We found that newborn DGCs of ASIC1a KO mouse at 28dpi (days post injection) had significantly shorter dendrites and smaller spine heads. Retroviral shRNA knockdown of ASIC1a in newborn DGCs induced the same phenotype as the ASIC1a KO mouse. Our results indicate that ASIC1a is necessary for dendritic development and synaptic organization of mouse hippocampal newborn neurons.