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Regenerating corticospinal fibers in the Marmoset ( Callitrix jacchus ) after spinal cord lesion and treatment with the anti‐Nogo‐A antibody IN‐1
Author(s) -
Fouad K.,
Klusman I.,
Schwab M. E.
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03716.x
Subject(s) - marmoset , corticospinal tract , sprouting , spinal cord , lesion , myelin , neurite , pathology , neuroscience , axon , regeneration (biology) , anatomy , medicine , central nervous system , biology , microbiology and biotechnology , magnetic resonance imaging , paleontology , biochemistry , botany , diffusion mri , in vitro , radiology
Neutralizing the myelin‐associated growth inhibitor Nogo‐A in adult spinal cord‐injured rats can promote regeneration of injured and compensatory sprouting of uninjured axons. Nogo‐A is present in humans, making its neutralization a possible novel treatment option for paraplegic patients. In this study we examined the effects of an extensively used anti‐Nogo‐A antibody (mAb IN‐1) on the regenerative capabilities of lesioned corticospinal tract (CST) axons in a primate, the Marmoset monkey. Unilateral thoracic lesions of the CST were performed in six adult Marmosets, followed by the application of mAb IN‐1 into the cerebrospinal fluid circulation by a graft of hybridoma cells. A unilateral injection of biotin dextran amine into the motor cortex was performed to analyse sprouting and regeneration of the lesioned axons. In the control antibody‐treated animal CST fibers stopped rostral to the lesion site and often showed retraction bulbs. In contrast, in four out of five mAb IN‐1‐treated animals fine labeled neurites had grown into, through and around the lesion site. Thus, this study provides first anatomical evidence that in primates, the neutralization of the myelin‐associated inhibitor Nogo‐A results in increased regenerative sprouting and growth of lesioned spinal cord axons.