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The Journal of Neuroscience, April 15, 2003, 23(8):3112

BRIEF COMMUNICATION
Inactivation of Myelin-Associated Glycoprotein Enhances Optic Nerve Regeneration

Eric V. Wong^{1, 3}, Samuel David², Michele H. Jacob¹, and Daniel G. Jay¹

¹ Departments of Physiology and Neuroscience, Tufts University Medical School, Boston, Massachusetts 02111, ² Center for Research in Neuroscience, Montreal General Hospital Research Institute and McGill University, Montreal, Quebec, Canada, and ³ Department of Biology, University of Louisville, Louisville Kentucky 40292

CNS regeneration in higher vertebrates is a long sought after goal in neuroscience. The lack of regeneration is attributable in part to inhibitory factors found in myelin (Caroni and Schwab, 1988a). Myelin-associated glycoprotein (MAG) is an abundant myelin protein that inhibits neurite outgrowth in vitro (McKerracher et al., 1994; Mukhopadhyay et al., 1994), but its role in regeneration remains controversial. To address this role, we performed nerve crush on embryonic day 15 chick retina-optic nerve explants and then acutely eliminated MAG function along the nerve using chromophore-assisted laser inactivation (CALI). CALI of MAG permitted significant regrowth of retinal axons past the site of lesion containing CNS myelin in contrast to various control treatments. Electron microscopy of the site of nerve crush shows abundant regenerating axons crossing the gap. When crushed optic nerve was retrogradely labeled at the nerve stump, no labeling of retinal neurons was observed. In contrast, labeling of CALI of MAG-treated crushed optic nerve showed significant retinal labeling (89 ± 16 cells per square millimeter), a value indistinguishable from that seen with non-crushed nerve (98 ± 13 cells per square millimeter). These findings implicate MAG as an important component of the myelin-derived inhibition of nerve regeneration. The acute loss of MAG function can promote significant axon growth across a site of CNS nerve damage.

Key words: MAG; CALI; optic nerve explants; nerve regeneration; retinal neurons; myelin

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Copyright © 2003 Society for Neuroscience  0270-6474/03/2383112-06$05.00/0

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				K. Venkatesh, O. Chivatakarn, S.-S. Sheu, and R. J. Giger Molecular dissection of the myelin-associated glycoprotein receptor complex reveals cell type-specific mechanisms for neurite outgrowth inhibition J. Cell Biol., May 7, 2007; 177(3): 393 - 399. [Abstract] [Full Text] [PDF]

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