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The Journal of Neuroscience, November 17, 2004, 24(46):10511-10520; doi:10.1523/JNEUROSCI.2828-04.2004

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Development/Plasticity/Repair
Blockade of Nogo-66, Myelin-Associated Glycoprotein, and Oligodendrocyte Myelin Glycoprotein by Soluble Nogo-66 Receptor Promotes Axonal Sprouting and Recovery after Spinal Injury

Shuxin Li,¹ Betty P. Liu,¹ Stephane Budel,¹ Mingwei Li,² Benxiu Ji,² Lee Walus,² Weiwei Li,² Adrienna Jirik,² Sylvia Rabacchi,² Eugene Choi,² Dane Worley,² Dinah W. Y. Sah,² Blake Pepinsky,² Daniel Lee,² Jane Relton,² and Stephen M. Strittmatter¹

¹Departments of Neurology and Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, and ²BiogenIdec, Inc., Cambridge, Massachusetts 02140

The growth of injured axons in the adult mammalian CNS is limited after injury. Three myelin proteins, Nogo, MAG (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), bind to the Nogo-66 receptor (NgR) and inhibit axonal growth in vitro. Transgenic or viral blockade of NgR function allows axonal sprouting in vivo. Here, we administered the soluble function-blocking NgR ectodomain [aa 27-310; NgR(310)ecto] to spinal-injured rats. Purified NgR(310)ecto-Fc protein was delivered intrathecally after midthoracic dorsal over-hemisection. Axonal sprouting of corticospinal and raphespinal fibers in NgR(310)ecto-Fc-treated animals correlates with improved spinal cord electrical conduction and improved locomotion. The ability of soluble NgR(310)ecto to promote axon growth and locomotor recovery demonstrates a therapeutic potential for NgR antagonism in traumatic spinal cord injury.

Key words: spinal cord; axon; Nogo; Nogo-66 receptor; serotonin; magnetic stimulation

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Received July 14, 2004; revised September 2, 2004; accepted October 13, 2004.

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