Role of L1CAM for axon sprouting and branching

The central nervous system (CNS) has been traditionally considered as an organ that fails to regenerate in response to injury. Indeed, the lesioned CNS faces a number of obstacles during regeneration, including an overall non-permissive environment for axonal regeneration. However, research during t...

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Bibliographic Details
Published in:Cell and tissue research 2012-07, Vol.349 (1), p.39-48
Main Authors: Schäfer, Michael K. E., Frotscher, Michael
Format: Article
Language:English
Subjects:
Analysis
Animals
Ankyrins - metabolism
Axons - metabolism
Axons - pathology
Biomedical and Life Sciences
Biomedicine
Cytoskeletal Proteins - metabolism
Human Genetics
Humans
Immunoglobulins
Injuries
Models, Biological
Molecular biology
Molecular Medicine
Nervous system
Neural Cell Adhesion Molecule L1 - chemistry
Neural Cell Adhesion Molecule L1 - metabolism
Neurobiology
Proteomics
Review
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Summary:The central nervous system (CNS) has been traditionally considered as an organ that fails to regenerate in response to injury. Indeed, the lesioned CNS faces a number of obstacles during regeneration, including an overall non-permissive environment for axonal regeneration. However, research during the last few decades has identified axon sprouting as an anatomical correlate for the regenerative capability of the CNS to establish new connections. The immunoglobulin superfamily member L1CAM has been shown to promote the capability of neurons for regenerative axon sprouting and to improve behavioral outcomes after CNS injury. Here, we discuss the cell-autonomous role of L1CAM for axon sprouting in experimental rodent injury models and highlight the molecular interactions of L1CAM with ankyrins, ezrin-radixin-moesin proteins and the Sema3A/Neuropilin ligand-receptor complex in the context of axonal branching.
ISSN:0302-766X
1432-0878
DOI:10.1007/s00441-012-1345-4