Toda Tomohisa, Hayakawa Itaru, Matsubayashi Yutaka, Tanaka Kenji, Ikenaka Kazuhiro, Lu Qing Richard, Kawasaki Hiroshi
Department of Molecular and Systems Neurobiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Mol Cell Neurosci. 2008 Sep;39(1):40-9. doi: 10.1016/j.mcn.2008.05.014. Epub 2008 Jul 9.
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.
发育可塑性的终止发生在发育过程中的特定时间点，但其背后的机制尚未完全明确。一种已被提出的假说是少突胶质细胞（OLs）发挥着重要作用。与此相符的是，我们发现OLs在触须损伤诱导的桶状结构可塑性关键期结束时出现在小鼠体感皮层中。为了验证这一假说，我们使用了两种OL分化存在缺陷的小鼠品系：Olig1基因敲除小鼠和jimpy小鼠。在Olig1基因敲除小鼠中，尽管完全没有OLs，但损伤诱导的可塑性终止并未延迟。即使通过药物治疗暂时阻断Olig1基因敲除小鼠的细胞构筑桶状结构形成，其终止时间仍正常。此外，jimpy小鼠的终止也未延迟。这些结果表明，尽管OLs在关键期结束时出现，但它们对于损伤诱导的可塑性终止并非内在必需。我们的研究结果强调了桶状皮层中丘脑皮质轴突可塑性终止与视觉皮层中丘脑皮质轴突可塑性终止之间的机制差异，最近有研究表明在视觉皮层中OL衍生的Nogo - A/B至关重要。
