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Regeneration‐enhancing effects of EphA4 blocking peptide following corticospinal tract injury in adult rat spinal cord
Author(s) -
Fabes Jez,
Anderson Patrick,
Brennan Caroline,
Bolsover Stephen
Publication year - 2007
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.1460-9568.2007.05859.x
Subject(s) - corticospinal tract , spinal cord injury , pyramidal tracts , spinal cord , neuroscience , axon , lesion , erythropoietin producing hepatocellular (eph) receptor , anatomy , biology , medicine , receptor , pathology , magnetic resonance imaging , diffusion mri , radiology , receptor tyrosine kinase
Spinal cord injury often leads to permanent incapacity because long axons cannot regenerate in the CNS. Eph receptors inhibit axon extension through an effect on the actin cytoskeleton. We have previously reported that after injury EphA4 appears at high levels in stumps of corticospinal axons, while a cognate ligand, ephrinB2, is upregulated at the lesion site so as to confine the injured axons. In this study we have infused lesioned spinal cords with a peptide antagonist of EphA4. In treated animals the retrograde degeneration that normally follows corticospinal tract injury is absent. Rather, corticospinal tract axons sprout up to and into the lesion centre. In a behavioural test of corticospinal tract function, peptide treatment substantially improved recovery relative to controls. These results suggest that blocking EphA4 is likely to contribute to a future successful clinical treatment for spinal cord injury.