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The Journal of Neuroscience, November 22, 2006, 26(47):12242-12250; doi:10.1523/JNEUROSCI.3827-06.2006

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Development/Plasticity/Repair
The Nogo–Nogo Receptor Pathway Limits a Spectrum of Adult CNS Axonal Growth

William B. J. Cafferty and Stephen M. Strittmatter

Program in Cellular Neuroscience, Neurodegeneration, and Repair, Yale University School of Medicine, New Haven, Connecticut 06510

Correspondence should be addressed to Stephen M. Strittmatter, Department of Neurology, Yale University School of Medicine, P.O. Box 208018, New Haven, CT 06510. Email: stephen.strittmatter{at}yale.edu

The hypothesis that Nogo-A (Reticulon 4A) and Nogo-66 receptor (NgR1) limit adult CNS axonal growth after injury is supported by both in vitro experiments and in vivo pharmacological studies. However, genetic assessment of the role of Nogo-A in corticospinal tract (CST) axons after spinal cord dorsal hemisection has yielded conflicting results. CST regeneration is detected in homozygous nogo-ab^trap/trap mice, but not in nogo-ab^atg/atg mice. CST regeneration is also present after pharmacological NgR blockade, but not in ngr1^–/– mice. To assess the nogo-ab^atg and ngr1-null alleles for other axon growth phenotypes, we created unilateral pyramidotomies and monitored the uninjured CST. There is robust pyramidotomy-induced growth of nogo-ab^atg/atg and ngr1^–/– CST axons into denervated cervical gray matter. This fiber growth correlates with recovery of fine motor skill in the affected forelimb. Thus nogo-ab and ngr1 play a modulated role in limiting CNS axonal growth across a spectrum of different tracts in various lesion models.

Key words: axon regeneration; corticospinal; Nogo; gene targeting; myelin; plasticity

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Received Sept. 2, 2006; revised Oct. 12, 2006; accepted Oct. 13, 2006.

Correspondence should be addressed to Stephen M. Strittmatter, Department of Neurology, Yale University School of Medicine, P.O. Box 208018, New Haven, CT 06510. Email: stephen.strittmatter{at}yale.edu

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