TY - JOUR
T1 - Termination of lesion-induced plasticity in the mouse barrel cortex in the absence of oligodendrocytes
AU - Toda, Tomohisa
AU - Hayakawa, Itaru
AU - Matsubayashi, Yutaka
AU - Tanaka, Kenji
AU - Ikenaka, Kazuhiro
AU - Lu, Qing Richard
AU - Kawasaki, Hiroshi
N1 - Funding Information:
We would like to thank Dr. Barbara Ranscht (The Burnham Institute) for generously providing the anti-GalC antibody. We are extremely grateful for Drs. Takuji Iwasato (RIKEN), Shoji Tsuji (The University of Tokyo), Yoshiki Sasai (RIKEN), Toshihide Yamashita (Chiba University) and Marc Tessier-Lavigne (Genentech Inc.) for the critical reading of this manuscript. We thank Tomoko Katayama, Yukari Ogasawara and Kaori Tanno for their excellent technical assistance. We thank Dr. Haruhiko Bito (The University of Tokyo), Bito lab members, and Kawasaki lab members for their helpful discussion and support. This work was supported by the 21st Century COE program “Center for Integrated Brain Medical Sciences” from MEXT, Grant-in-Aid for Scientific Research on Priority Areas-Elucidation of neural network function in the brain from MEXT, and PRESTO from Japan Science and Technology Agency. This work was also supported by Inamori Foundation and Takeda Science Foundation.
PY - 2008/9
Y1 - 2008/9
N2 - 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.
AB - 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.
KW - Barrel plasticity
KW - Critical period
KW - Olig1
KW - Somatosensory cortex
KW - Thalamocortical projection
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U2 - 10.1016/j.mcn.2008.05.014
DO - 10.1016/j.mcn.2008.05.014
M3 - Article
C2 - 18588982
AN - SCOPUS:49549095980
SN - 1044-7431
VL - 39
SP - 40
EP - 49
JO - Molecular and Cellular Neuroscience
JF - Molecular and Cellular Neuroscience
IS - 1
ER -