GABA-B1 Receptor-Null Schwann Cells Exhibit Compromised In Vitro Myelination

GABA-B receptors are important for Schwann cell (SC) commitment to a non-myelinating phenotype during development. However, the P0-GABA-B1 fl/fl conditional knockout mice, lacking the GABA-B1 receptor specifically in SCs, also presented axon modifications, suggesting SC non-autonomous effects throug...

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Bibliographic Details
Published in:Molecular neurobiology 2019-02, Vol.56 (2), p.1461-1474
Main Authors: Faroni, Alessandro, Melfi, Simona, Castelnovo, Luca Franco, Bonalume, Veronica, Colleoni, Deborah, Magni, Paolo, Araúzo-Bravo, Marcos J., Reinbold, Rolland, Magnaghi, Valerio
Format: Article
Language:English
Subjects:
Animals
Axons - metabolism
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cells, Cultured
Clonal deletion
Dorsal root ganglia
gamma-Aminobutyric Acid - metabolism
Ganglia, Spinal - cytology
Mice
Mice, Transgenic
Myelin P0 protein
Myelin Sheath - metabolism
Myelination
Neurobiology
Neurology
Neurons - metabolism
Neurosciences
Neurotransmitters
Phenotypes
Receptors, GABA-B - deficiency
Schwann cells
Schwann Cells - cytology
Sensory neurons
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Summary:GABA-B receptors are important for Schwann cell (SC) commitment to a non-myelinating phenotype during development. However, the P0-GABA-B1 fl/fl conditional knockout mice, lacking the GABA-B1 receptor specifically in SCs, also presented axon modifications, suggesting SC non-autonomous effects through the neuronal compartment. In this in vitro study, we evaluated whether the specific deletion of the GABA-B1 receptor in SCs may induce autonomous or non-autonomous cross-changes in sensory dorsal root ganglia (DRG) neurons. To this end, we performed an in vitro biomolecular and transcriptomic analysis of SC and DRG neuron primary cultures from P0-GABA-B1 fl/fl mice. We found that cells from conditional P0-GABA-B1 fl/fl mice exhibited proliferative, migratory and myelinating alterations. Moreover, we found transcriptomic changes in novel molecules that are involved in peripheral neuron–SC interaction.
ISSN:0893-7648
1559-1182
DOI:10.1007/s12035-018-1158-x