Termination of lesion-induced plasticity in the mouse barrel cortex in the absence of oligodendrocytes

Tomohisa Toda, Itaru Hayakawa, Yutaka Matsubayashi, Kenji Tanaka, Kazuhiro Ikenaka, Qing Richard Lu, Hiroshi Kawasaki

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


Termination of developmental plasticity occurs at specific points in development, and the mechanisms responsible for it are not well understood. One hypothesis that has been proposed is that oligodendrocytes (OLs) play an important role. Consistent with this, we found that OLs appeared in the mouse somatosensory cortex at the end of the critical period for whisker lesion-induced barrel structural plasticity. To test this hypothesis, we used two mouse lines with defective OL differentiation: Olig1-deficient and jimpy. In Olig1-deficient mice, although OLs were totally absent, the termination of lesion-induced plasticity was not delayed. The timing was normal even when the cytoarchitectonic barrel formation was temporarily blocked by pharmacological treatment in Olig1-deficient mice. Furthermore, the termination was not delayed in jimpy mice. These results demonstrate that, even though OLs appear at the end of the critical period, OLs are not intrinsically necessary for the termination of lesion-induced plasticity. Our findings underscore a mechanistic distinction between the termination of thalamocortical axonal plasticity in the barrel cortex and that in the visual cortex, in which OL-derived Nogo-A/B was recently suggested to be essential.

Original languageEnglish
Pages (from-to)40-49
Number of pages10
JournalMolecular and Cellular Neuroscience
Issue number1
Publication statusPublished - 2008 Sept
Externally publishedYes


  • Barrel plasticity
  • Critical period
  • Olig1
  • Somatosensory cortex
  • Thalamocortical projection

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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