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The Journal of Neuroscience, January 30, 2008, 28(5):1099-1108; doi:10.1523/JNEUROSCI.4906-07.2008

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Cellular/Molecular
Netrin-1 Is a Novel Myelin-Associated Inhibitor to Axon Growth

Karin Löw,1 Maya Culbertson,1 Frank Bradke,2 Marc Tessier-Lavigne,2 and Mark H. Tuszynski1,3

1Department of Neurosciences, University of California-San Diego, La Jolla, California 92093, 2Department of Biological Sciences, Howard Hughes Medical Institute, Stanford University, Palo Alto, California 94305, and 3Veterans Affairs Medical Center, San Diego, California 92161

Correspondence should be addressed to Karin Löw, Department of Neurosciences, University of California, San Diego, Basic Science Building, Room 4046, 9500 Gilman Drive, La Jolla, CA 92093. Email: kloew{at}ucsd.edu

We investigated the influence of the bifunctional guidance molecule netrin-1 on axonal growth in the injured adult spinal cord. In the adult, netrin-1 is expressed on mature oligodendrocytes, cells of the central canal, and the meninges. Netrin-1 protein in white matter is selectively enriched adjacent to paranodal loops of myelin in nodes of Ranvier. The repulsion-mediating netrin-1 uncoordinated-5 (UNC5) receptors are expressed by neurons of the corticospinal and rubrospinal projections, and by intrinsic neurons of the spinal cord, both before and after spinal cord injury. Neutralization of netrin-1 in myelin prepared from adult rat spinal cord using UNC5 receptor bodies increases neurite outgrowth from UNC5-expressing spinal motor neurons in vitro. Furthermore, axon regeneration is inhibited in a netrin-1-enriched zone, devoid of other myelin-associated inhibitors, within spinal cord lesion sites in vivo. We conclude that netrin-1 is a novel oligodendrocyte-associated inhibitor that can contribute to axonal growth failure after adult spinal cord injury.

Key words: spinal cord injury; axon regeneration; white matter inhibition; netrin-1; UNC5; DCC; nogo; MAG; OMgp; retrovirus; plasticity; corticospinal; rubrospinal; intraspinal

Received June 7, 2007; accepted Dec. 1, 2007.

Correspondence should be addressed to Karin Löw, Department of Neurosciences, University of California, San Diego, Basic Science Building, Room 4046, 9500 Gilman Drive, La Jolla, CA 92093. Email: kloew{at}ucsd.edu






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