% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Li:256611,
      author       = {Li, Kaizhen and Figarella, Katherine and Su, Xin and
                      Kovalchuk, Yury and Gorzolka, Jessika and Neher, Jonas J and
                      Mojtahedi, Nima and Casadei, Nicolas and Hedrich, Ulrike B S
                      and Garaschuk, Olga},
      title        = {{E}ndogenous but not sensory-driven activity controls
                      migration, morphogenesis and survival of adult-born
                      juxtaglomerular neurons in the mouse olfactory bulb.},
      journal      = {Cellular and molecular life sciences},
      volume       = {80},
      number       = {4},
      issn         = {1420-682X},
      address      = {Cham (ZG)},
      publisher    = {Springer International Publishing AG},
      reportid     = {DZNE-2023-00363},
      pages        = {98},
      year         = {2023},
      note         = {CC BY},
      abstract     = {The development and survival of adult-born neurons are
                      believed to be driven by sensory signaling. Here, in vivo
                      analyses of motility, morphology and Ca2+ signaling, as well
                      as transcriptome analyses of adult-born juxtaglomerular
                      cells with reduced endogenous excitability (via
                      cell-specific overexpression of either Kv1.2 or Kir2.1 K+
                      channels), revealed a pronounced impairment of migration,
                      morphogenesis, survival, and functional integration of these
                      cells into the mouse olfactory bulb, accompanied by a
                      reduction in cytosolic Ca2+ fluctuations, phosphorylation of
                      CREB and pCREB-mediated gene expression. Moreover, K+
                      channel overexpression strongly downregulated genes involved
                      in neuronal migration, differentiation, and morphogenesis
                      and upregulated apoptosis-related genes, thus locking
                      adult-born cells in an immature and vulnerable state.
                      Surprisingly, cells deprived of sensory-driven activity
                      developed normally. Together, the data reveal signaling
                      pathways connecting the endogenous intermittent neuronal
                      activity/Ca2+ fluctuations as well as enhanced Kv1.2/Kir2.1
                      K+ channel function to migration, maturation, and survival
                      of adult-born neurons.},
      keywords     = {Mice / Animals / Olfactory Bulb: metabolism / Neurons:
                      metabolism / Neurogenesis: genetics / Cell Differentiation /
                      Cell Movement / Adult neurogenesis (Other) / Differentiation
                      (Other) / Endogenous activity (Other) / Migration (Other) /
                      Neuronal development (Other) / Olfactory bulb (Other) /
                      Potassium channels (Other) / Spontaneous calcium transients
                      (Other) / Survival (Other) / pCREB (Other)},
      cin          = {AG Neher},
      ddc          = {610},
      cid          = {I:(DE-2719)1210012},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36932186},
      pmc          = {pmc:PMC10023654},
      doi          = {10.1007/s00018-023-04753-4},
      url          = {https://pub.dzne.de/record/256611},
}