Adult neurogenesis arises from neural stem cells within specialized niches.Neuronal activity and experience,presumably acting upon this local niche,regulate multiple stages of adult neurogenesis,from quiescent neural stem cell activation and neural progenitor proliferation to new neuron maturation,synaptic integration and survival.The niche mechanism that couples neuronal circuitry activity to regulate distinct stages of adult neurogenesis is largely unknown.Our recent optogenetic analysis identified parvalbumin-expressing(PV+)interneurons as a critical and unique niche component among different interneuron subtypes that couples neuronal circuit activity to regulate radial glia-like neural stem cell decision between quiescence and activation in vivo under both physiological conditions and in response to specific experience.In contrast to the inhibitory role on quiescent radial glia-like neural stem cell activation,PV+ interneuron activity positively regulates proliferating neuronal progeny survival.Specifically,we show that proliferating neuronal precursors in the adult mouse dentate gyrus exhibit immature GABAergic synaptic inputs originating from local PV+ interneurons.Moreover,PV+ interneurons promote survival of proliferative newborn progeny during early phases of adult hippocampal neurogenesis upon optogenetic activation,whereas their suppression leads to decreased newborn progeny survival under both basal and enriched environment conditions.Our study identifies a novel niche mechanism involving PV+ interneurons that couples local circuit activity to diametric regulation of quiescent neural stem cell activation and survival of their proliferating neuronal progeny,two sequential phases of adult hippocampal neurogenesis.