PDGFRA/NG2 glia generate myelinating oligodendrocytes and piriform projection neurons in adult mice

By L. Rivers, K. Young, M. Rizzi, F. Jamen, K. Psachoulia, A. Wade, N. Kessaris, W. Richardson. Nature Neuroscience, 2008

945 citations recorded by the source corpus.

Platelet-derived growth factor α receptor (PDGFRA)/NG2–expressing glia are distributed throughout the adult CNS. They are descended from oligodendrocyte precursors (OLPs) in the perinatal CNS, but it is not clear whether they continue to generate myelinating oligodendrocytes or other differentiated cells during normal adult life. We followed the fates of adult OLPs in Pdgfra-creERT2/Rosa26-YFP double-transgenic mice and found that they generated many myelinating oligodendrocytes during adulthood; >20% of all oligodendrocytes in the adult mouse corpus callosum were generated after 7 weeks of age, raising questions about the function of the late-myelinating axons. OLPs also produced some myelinating cells in the cortex, but the majority of adult-born cortical cells did not appear to myelinate. We found no evidence for astrocyte production in gray or white matter. However, small numbers of projection neurons were generated in the forebrain, especially in the piriform cortex, which is the main target of the olfactory bulb.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/605bd2e2f5c5cc3d583dca453b120c581b7fdaf2

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Citations in the corpus

Origin of new glial cells in intact and injured adult spinal cord. (2010, background): “White matter astrocytes expressed Sox9 and high levels of GFAP, but not Olig2.”
In vivo identification of bipotential adipocyte progenitors recruited by β3-adrenoceptor activation and high fat feeding (2012, neutral): “In one series of experi- ments, we crossed Cre-responsive (stop codon-floxed) reporter mice (Madisen et al., 2010) with mice expressing tamoxifeninducible CreERT2 under the control of PDGFRa promoter (Rivers et al., 2008) (Figure 4A).”
The Glial Nature of Embryonic and Adult Neural Stem Cells (2009, background): “Oligodendrocyte progenitor cells (generally referred to as OPCs) are NG2-expressing proliferating cells distributed throughout the brain (Noble 2000, Aguirre et al. 2007, Barres 2008, Rivers et al. 2008).”
Heterogeneity of Astrocytic Form and Function (2012, neutral): “Other studies using similar cell fate mapping strategy based upon the expression of PDGFα identified derived oligodendrocytes and additional NG2 cells, as well as small numbers of pyriform neurons, yet failed to see astrocytes in grey or white matter (53).”
Oligodendrocyte Dynamics in the Healthy Adult CNS: Evidence for Myelin Remodeling (2013, positive): “Transgenic Mice and Cre Recombination Homozygous Pdgfra-CreER BAC transgenic mice (Rivers et al., 2008) were crossed with Cre-sensitive reporter mice—either homozygous Rosa26RYFP (R26R-YFP) reporters (Srinivas et al.”
Leptin Receptor-expressing mesenchymal stromal cells represent the main source of bone formed by adult bone marrow (2014, neutral): “PDGFRa+ bone marrow cells are thus highly enriched for CFU-F, but we could not fate map PDGFRa+ cells because Pdgfra-CreER (Rivers et al., 2008) recombined poorly in bone marrow PDGFRa+ cells (data not shown).”
NG2+ CNS glial progenitors remain committed to the oligodendrocyte lineage in postnatal life and following neurodegeneration. (2010, methodology): “…cells in both regions retain the capacity to proliferate and generate OLs, suggesting that NG2+ cells are not intrinsically heterogeneous with regard to their ability to divide and differentiate, as previously suggested (Bouslama-Oueghlani et al., 2005; Dimou et al., 2008; Rivers et al., 2008).”
CNS-Resident Glial Progenitor/Stem Cells Produce Schwann Cells as well as Oligodendrocytes during Repair of CNS Demyelination (2010, neutral): “…lesion, where oligodendrocyte-mediated remyelination can be detected by histology ( cells of oligodendrocyte morphology expressing CC1 in the normal appearing white matter remote from the lesion and in intact gray matter (data not shown), consistent with our earlier findings (Rivers et al., 2008).”