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Experience-dependent regulation of NG2 progenitors in the developing barrel cortex

Abstract

We found that, during the formation of the mouse barrel cortex, NG2 cells received glutamatergic synapses from thalamocortical fibers and preferentially accumulated along septa separating the barrels. Sensory deprivation reduced thalamocortical inputs on NG2 cells and increased their proliferation, leading to a more uniform distribution in the deprived barrels. Thus, early sensory experience regulates thalamocortical innervation on NG2 cells, as well as their proliferation and distribution during development.

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Figure 1: NG2+ progenitors are functionally innervated by thalamocortical glutamatergic synapses and accumulate at the border between cortical barrels.
Figure 2: Whisker lesion at birth alters the density of NG2+ cells in the barrel fields.
Figure 3: Location in the barrel field and sensory experience regulate the thalamocortical innervation and proliferation rate of NG2+ progenitor cells.

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References

  1. Dawson, M.R., Polito, A., Levine, J.M. & Reynolds, R. Mol. Cell. Neurosci. 24, 476–488 (2003).

    Article  CAS  PubMed  Google Scholar 

  2. Mangin, J.M. & Gallo, V. ASN Neuro. 3, e00052 (2011).

    PubMed  PubMed Central  Google Scholar 

  3. Kukley, M. et al. FASEB J. 22, 2957–2969 (2008).

    Article  CAS  PubMed  Google Scholar 

  4. Ge, W.P., Zhou, W., Luo, Q., Jan, L.Y. & Jan, Y.N. Proc. Natl. Acad. Sci. USA 106, 328–333 (2009).

    Article  CAS  PubMed  Google Scholar 

  5. Tanaka, Y. et al. Cereb. Cortex 19, 2181–2195 (2009).

    Article  PubMed  Google Scholar 

  6. Daw, M.I., Ashby, M.C. & Isaac, J.T. Nat. Neurosci. 10, 453–461 (2007).

    Article  CAS  PubMed  Google Scholar 

  7. Laurent, A. et al. J. Neurosci. 22, 886–900 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Erzurumlu, R.S. & Kind, P.C. Trends Neurosci. 24, 589–595 (2001).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Houades, V., Koulakoff, A., Ezan, P., Seif, I. & Giaume, C. J. Neurosci. 28, 5207–5217 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Erzurumlu, R.S. & Jhaveri, S. Brain Res. Dev. Brain Res. 56, 229–234 (1990).

    Article  CAS  PubMed  Google Scholar 

  11. Datwani, A. et al. J. Neurosci. 22, 9171–9175 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Finnerty, G.T., Roberts, L.S. & Connors, B.W. Nature 400, 367–371 (1999).

    Article  CAS  PubMed  Google Scholar 

  13. Yuan, X. et al. Development 125, 2901–2914 (1998).

    CAS  PubMed  Google Scholar 

  14. Gudz, T.I., Komuro, H. & Macklin, W.B. J. Neurosci. 26, 2458–2466 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Jain, N. et al. J Neurosci. 23, 10321–10330 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Yuan, X. et al. J. Neurosci. Res. 70, 529–545 (2002).

    Article  CAS  PubMed  Google Scholar 

  17. Mangin, J.M., Kunze, A., Chittajallu, R. & Gallo, V. J. Neurosci. 28, 7610–7623 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Sugiyama, S. et al. Cell 134, 508–520 (2008).

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

We thank D. Bergles and M. Huntsman for discussion. We thank L.-J. Chew, J. Corbin, M. Huntsman and J. Liu for critically reading an earlier version of this manuscript. We thank E. Quinlan (University of Maryland) for her advice on the dark-rearing experiments. We also thank R. Chittajallu and J. Isaac for their help with the thalamocortical slice preparation. This work was supported by grants from the US National Institutes of Health (NIH; R01NS045702, R01NS056427) and NIH Intellectual and Developmental Disabilities Research Center (P30HD40677) to V.G., an NIH grant (K08NS073793) to J.S., and by Agence Nationale de la Recherche Jeune Chercheuse Jeune Chercheur Grant Oligospine (J.-M.M.).

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J.-M.M. designed and performed all of the experiments and analyzed the data. P.L. and J.S. performed the dark-rearing experiments and analyzed the data. V.G. participated in the design of the experiments, supervised the project and wrote the manuscript with J.-M.M.

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Correspondence to Jean-Marie Mangin or Vittorio Gallo.

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The authors declare no competing financial interests.

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Mangin, JM., Li, P., Scafidi, J. et al. Experience-dependent regulation of NG2 progenitors in the developing barrel cortex. Nat Neurosci 15, 1192–1194 (2012). https://doi.org/10.1038/nn.3190

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