Motor training compensates for cerebellar dysfunctions caused by oligodendrocyte ablation

被引:18
作者
Collin, L [1 ]
Usiello, A [1 ]
Erbs, E [1 ]
Mathis, C [1 ]
Borrelli, E [1 ]
机构
[1] Univ Louis Pasteur Strasbourg 1, INSERM,CNRS, Dept Mol Neurobiol, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France
关键词
D O I
10.1073/pnas.0305994101
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The role played by oligodendrocytes (OLs), the myelinating cells of the CNS, during brain development has not been fully explored. We have addressed this question by inducing a temporal and reversible ablation of OLs on postnatal CNS development. OL ablation in newborn mice leads to a profound alteration in the structure of the cerebellar cortex, which can be progressively rescued by newly generated cells, leading to a delayed myelination. Nevertheless, the temporal shift of the OL proliferation and myelinating program cannot completely compensate for developmental defects, resulting in impaired motor functions in the adult. Strikingly, we show that, despite these abnormalities, epigenetic factors, such as motor training, are able to fully rescue cerebellar-directed motor skills.
引用
收藏
页码:325 / 330
页数:6
相关论文
共 31 条
[1]   Ataxia and abnormal cerebellar microorganization in mice with ablated contactin gene expression [J].
Berglund, EO ;
Murai, KK ;
Fredette, B ;
Sekerková, G ;
Marturano, B ;
Weber, L ;
Mugnaini, E ;
Ranscht, B .
NEURON, 1999, 24 (03) :739-750
[2]   LEARNING CAUSES SYNAPTOGENESIS, WHEREAS MOTOR-ACTIVITY CAUSES ANGIOGENESIS, IN CEREBELLAR CORTEX OF ADULT-RATS [J].
BLACK, JE ;
ISAACS, KR ;
ANDERSON, BJ ;
ALCANTARA, AA ;
GREENOUGH, WT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (14) :5568-5572
[3]   TRANSGENIC MICE WITH INDUCIBLE DWARFISM [J].
BORRELLI, E ;
HEYMAN, RA ;
ARIAS, C ;
SAWCHENKO, PE ;
EVANS, RM .
NATURE, 1989, 339 (6225) :538-541
[4]   TARGETING OF AN INDUCIBLE TOXIC PHENOTYPE IN ANIMAL-CELLS [J].
BORRELLI, E ;
HEYMAN, R ;
HSI, M ;
EVANS, RM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (20) :7572-7576
[5]   Myelination in the absence of galactolipids and proteolipid proteins [J].
Coetzee, T ;
Suzuki, K ;
Nave, KA ;
Popko, B .
MOLECULAR AND CELLULAR NEUROSCIENCE, 1999, 14 (01) :41-51
[6]  
Delaney CL, 1996, J NEUROSCI, V16, P6908
[7]   The cells and molecules that make a cerebellum [J].
Goldowitz, D ;
Hamre, K .
TRENDS IN NEUROSCIENCES, 1998, 21 (09) :375-382
[8]   Axonal swellings and degeneration in mice lacking the major proteolipid of myelin [J].
Griffiths, I ;
Klugmann, M ;
Anderson, T ;
Yool, D ;
Thomson, C ;
Schwab, MH ;
Schneider, A ;
Zimmermann, F ;
McCulloch, M ;
Nadon, N ;
Nave, KA .
SCIENCE, 1998, 280 (5369) :1610-1613
[9]   Myelin mutants: Model systems for the study of normal and abnormal myelination [J].
Griffiths, IR .
BIOESSAYS, 1996, 18 (10) :789-797
[10]   Microdomains for neuron-glia interaction:: parallel fiber signaling to Bergmann glial cells [J].
Grosche, J ;
Matyash, V ;
Möller, T ;
Verkhratsky, A ;
Reichenbach, A ;
Kettenmann, H .
NATURE NEUROSCIENCE, 1999, 2 (02) :139-143