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@ARTICLE{SchneiderLdi:283102,
      author       = {Schneider-Lódi, Mária and Ahrari, Ala and Meseke, Maurice
                      and Corvace, Franco and Kümmel, Marie-Luise and Trampe,
                      Anne-Kathrin and Hamad, Mohammad I K and Förster, Eckart},
      title        = {{E}arly {P}ostnatally {I}nduced {C}onditional {R}eelin
                      {D}eficiency {C}auses {M}alformations of {H}ippocampal
                      {N}eurons.},
      journal      = {Biomolecules},
      volume       = {15},
      number       = {12},
      issn         = {2218-273X},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DZNE-2025-01509},
      pages        = {1662},
      year         = {2025},
      abstract     = {The extracellular matrix protein reelin is well known for
                      orchestrating radial migration of cortical neurons during
                      embryonic cortical development. While in the reeler mutant
                      mouse, lacking reelin expression, radially migrating neurons
                      are malpositioned and display dendritic malformations, no
                      such deficits were found after conditionally induced reelin
                      deficiency (RelncKO) in the hippocampus of mice aged two
                      months. Here, we addressed the question whether or not
                      RelncKO, when induced early after birth, might cause
                      malformations of hippocampal neurons. For instance, we could
                      recently show dendritic hypertrophy of somatosensory and
                      entorhinal cortex neurons after early induced RelncKO. In
                      the present study, reelin deficiency in RelncKO mice was
                      induced immediately after birth, and the analysis of
                      reconstructed Golgi-stained hippocampal neurons from these
                      mice, when aged 4 weeks, revealed morphological
                      malformations. Dentate granule cells were the most affected
                      from all analyzed hippocampal neuronal cell types. Thus,
                      RelncKO granule cells had a significantly smaller soma size
                      and displayed atrophy of proximal dendritic segments when
                      compared to wild type (wt). Malformations of interneurons
                      were only subtle and cell type specific; thus, multipolar
                      but not bitufted interneurons developed proximal dendritic
                      hypertrophy. Also, the dendrite morphology of CA2- and
                      CA3-pyramidal cells was affected, while we did not detect
                      morphological changes of CA1-pyramidal cell dendrites. In
                      summary, our results show that early postnatal RelncKO
                      causes morphological malformations of hippocampal neurons,
                      in particular of dentate granule cells. Taken together with
                      our previous findings, we conclude that not only specific
                      types of entorhinal- and neocortical neurons, but also types
                      of hippocampal neurons are at risk of developing
                      malformations if reelin expression is reduced during a
                      critical early postnatal period.},
      keywords     = {Animals / Reelin Protein / Hippocampus: metabolism /
                      Hippocampus: pathology / Serine Endopeptidases: deficiency /
                      Serine Endopeptidases: genetics / Serine Endopeptidases:
                      metabolism / Cell Adhesion Molecules, Neuronal: deficiency /
                      Cell Adhesion Molecules, Neuronal: genetics / Cell Adhesion
                      Molecules, Neuronal: metabolism / Nerve Tissue Proteins:
                      deficiency / Nerve Tissue Proteins: genetics / Nerve Tissue
                      Proteins: metabolism / Extracellular Matrix Proteins:
                      deficiency / Extracellular Matrix Proteins: genetics /
                      Extracellular Matrix Proteins: metabolism / Mice / Neurons:
                      metabolism / Neurons: pathology / Mice, Knockout /
                      Dendrites: metabolism / Dendrites: pathology / dendritic
                      morphology (Other) / granule cells (Other) / hippocampus
                      (Other) / interneurons (Other) / knock-out (Other) / neuron
                      reconstruction (Other) / pyramidal cells (Other) / reelin
                      (Other) / silver staining (Other) / Reelin Protein (NLM
                      Chemicals) / Reln protein, mouse (NLM Chemicals) / Serine
                      Endopeptidases (NLM Chemicals) / Cell Adhesion Molecules,
                      Neuronal (NLM Chemicals) / Nerve Tissue Proteins (NLM
                      Chemicals) / Extracellular Matrix Proteins (NLM Chemicals)},
      cin          = {AG Salomoni},
      ddc          = {570},
      cid          = {I:(DE-2719)1013032},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41463318},
      doi          = {10.3390/biom15121662},
      url          = {https://pub.dzne.de/record/283102},
}