Development of the corticospinal tract in semaphorin3A-and CD24-deficient mice

被引:13
作者
Sibbe, M. [1 ]
Taniguchi, M. [2 ]
Schachner, M. [3 ,4 ]
Bartsch, U. [1 ]
机构
[1] Univ Hamburg, Med Ctr, Dept Ophthalmol, D-20246 Hamburg, Germany
[2] Sapporo Med Univ, Sch Med, Canc Res Inst, Dept Biochem, Sapporo, Hokkaido 0608556, Japan
[3] Univ Hamburg, Zentrum Mol Neurobiol, D-20251 Hamburg, Germany
[4] Rutgers State Univ, Keck Ctr Collaborat Neurosci, Dept Cell Biol & Neurosci, New Brunswick, NJ 08901 USA
关键词
axonal path finding; anterogracle axonal tracing; L1; pyramidal decussation; spinal cord;
D O I
10.1016/j.neuroscience.2007.10.007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mutations in the gene encoding the neural recognition molecule L1 result in hypoplasia of the corticospinal tract and path finding errors of corticospinal axons at the pyramidal decussation. Candidate molecules that have been implicated in L1-dependent guidance of corticospinal axons from the ventral medullary pyramids to the contralateral dorsal columns of the cervical spinal cord include Semaphorin3A and CD24. In the present study, we anterogradely labeled corticospinal axons from the sensorimotor cortex of young postnatal Semaphorin3A- and CD24-cleficient mice to elucidate potential functions of both proteins during formation of this long axon projection. Our results indicate that elongation, collateralization, fasciculation and path finding of corticospinal axons in mice proceed normally in the absence of Semaphorin3A or CD24. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:898 / 904
页数:7
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