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Neuron. 2003 Apr 24;38(2):187-99.

Axon regeneration in young adult mice lacking Nogo-A/B.

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  • 1Department of Neurology, Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.

Abstract

After injury, axons of the adult mammalian brain and spinal cord exhibit little regeneration. It has been suggested that axon growth inhibitors, such as myelin-derived Nogo, prevent CNS axon repair. To investigate this hypothesis, we analyzed mice with a nogo mutation that eliminates Nogo-A/B expression. These mice are viable and exhibit normal locomotion. Corticospinal tract tracing reveals no abnormality in uninjured nogo-A/B(-/-) mice. After spinal cord injury, corticospinal axons of young adult nogo-A/B(-/-) mice sprout extensively rostral to a transection. Numerous fibers regenerate into distal cord segments of nogo-A/B(-/-) mice. Recovery of locomotor function is improved in these mice. Thus, Nogo-A plays a role in restricting axonal sprouting in the young adult CNS after injury.

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PMID:
12718854
[PubMed - indexed for MEDLINE]
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