RNA seq profile of adult newborn neurons

The integration of adult-born neurons in the existent neural circuitry is known to be activity-dependent. To decipher the underlying mechanisms, we genetically manipulated excitability of adult-born cells (via cell-specific overexpression of either Kv1.2 or Kir2.1 K+ channels). Longitudinal in vivo Ca2+ imaging and transcriptome analyses revealed that endogenous but not sensory-driven activity governs migration, morphogenesis, survival, and functional integration of adult-born juxtaglomerular neurons in the mouse olfactory bulb. The proper development of these cells required fluctuations of cytosolic Ca2+ levels, phosphorylation of CREB, and pCREB-mediated gene expression. Attenuating Ca2+ fluctuations via K+ channel overexpression strongly downregulated genes involved in neuronal migration, differentiation, and morphogenesis and upregulated the apoptosis-related genes, thus locking adult-born cells in the vulnerable and immature state. Together, the data identify signaling pathways connecting the endogenous intermittent neuronal activity/Ca2+ fluctuations as well as proper Kv1.2/Kir2.1 K+ channel function to migration, maturation, and survival of adult-born neurons. Overall design: we used 12 male 3 months-old mice and split them into three groups, namely control NBNs, Kv1.2-overexpressing NBNs, and Kir2.1-overexpressing NBNs. The 4 mice in each group were further divided into two subgroups to have 2 biological replicates in each group. For each sample, NBNs from two mice were pooled together. In total, we analyzed 6 samples.