Home > Publications Database > Early Postnatally Induced Conditional Reelin Deficiency Causes Malformations of Hippocampal Neurons. > print

001     283102
005     20260217130126.0
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|a pmc:PMC12730948
024 7 _ |2 doi
|a 10.3390/biom15121662
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|a pmid:41463318
037 _ _ |a DZNE-2025-01509
041 _ _ |a English
082 _ _ |a 570
100 1 _ |0 0000-0002-6533-770X
|a Schneider-Lódi, Mária
|b 0
245 _ _ |a Early Postnatally Induced Conditional Reelin Deficiency Causes Malformations of Hippocampal Neurons.
260 _ _ |a Basel
|b MDPI
|c 2025
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520 _ _ |a 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.
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650 _ 7 |2 Other
|a dendritic morphology
650 _ 7 |2 Other
|a granule cells
650 _ 7 |2 Other
|a hippocampus
650 _ 7 |2 Other
|a interneurons
650 _ 7 |2 Other
|a knock-out
650 _ 7 |2 Other
|a neuron reconstruction
650 _ 7 |2 Other
|a pyramidal cells
650 _ 7 |2 Other
|a reelin
650 _ 7 |2 Other
|a silver staining
650 _ 7 |2 NLM Chemicals
|a Reelin Protein
650 _ 7 |0 EC 3.4.21.-
|2 NLM Chemicals
|a Reln protein, mouse
650 _ 7 |0 EC 3.4.21.-
|2 NLM Chemicals
|a Serine Endopeptidases
650 _ 7 |2 NLM Chemicals
|a Cell Adhesion Molecules, Neuronal
650 _ 7 |2 NLM Chemicals
|a Nerve Tissue Proteins
650 _ 7 |2 NLM Chemicals
|a Extracellular Matrix Proteins
650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Reelin Protein
650 _ 2 |2 MeSH
|a Hippocampus: metabolism
650 _ 2 |2 MeSH
|a Hippocampus: pathology
650 _ 2 |2 MeSH
|a Serine Endopeptidases: deficiency
650 _ 2 |2 MeSH
|a Serine Endopeptidases: genetics
650 _ 2 |2 MeSH
|a Serine Endopeptidases: metabolism
650 _ 2 |2 MeSH
|a Cell Adhesion Molecules, Neuronal: deficiency
650 _ 2 |2 MeSH
|a Cell Adhesion Molecules, Neuronal: genetics
650 _ 2 |2 MeSH
|a Cell Adhesion Molecules, Neuronal: metabolism
650 _ 2 |2 MeSH
|a Nerve Tissue Proteins: deficiency
650 _ 2 |2 MeSH
|a Nerve Tissue Proteins: genetics
650 _ 2 |2 MeSH
|a Nerve Tissue Proteins: metabolism
650 _ 2 |2 MeSH
|a Extracellular Matrix Proteins: deficiency
650 _ 2 |2 MeSH
|a Extracellular Matrix Proteins: genetics
650 _ 2 |2 MeSH
|a Extracellular Matrix Proteins: metabolism
650 _ 2 |2 MeSH
|a Mice
650 _ 2 |2 MeSH
|a Neurons: metabolism
650 _ 2 |2 MeSH
|a Neurons: pathology
650 _ 2 |2 MeSH
|a Mice, Knockout
650 _ 2 |2 MeSH
|a Dendrites: metabolism
650 _ 2 |2 MeSH
|a Dendrites: pathology
700 1 _ |0 P:(DE-2719)9002127
|a Ahrari, Ala
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700 1 _ |a Meseke, Maurice
|b 2
700 1 _ |a Corvace, Franco
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700 1 _ |a Kümmel, Marie-Luise
|b 4
700 1 _ |a Trampe, Anne-Kathrin
|b 5
700 1 _ |0 0000-0002-7413-0305
|a Hamad, Mohammad I K
|b 6
700 1 _ |0 0000-0002-2478-5610
|a Förster, Eckart
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773 _ _ |0 PERI:(DE-600)2701262-1
|a 10.3390/biom15121662
|g Vol. 15, no. 12, p. 1662 -
|n 12
|p 1662
|t Biomolecules
|v 15
|x 2218-273X
|y 2025
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