Chondroitinase ABC promotes functional recovery after spinal cord injury

Elizabeth J. Bradbury (), Lawrence D. F. Moon, Reena J. Popat, King Von R., Gavin S. Bennett, Preena N. Patel, James W. Fawcett and Stephen B. McMahon
Additional contact information
Elizabeth J. Bradbury: Hodgkin Building, Kings College London, Guy's Campus
Lawrence D. F. Moon: University of Cambridge
Reena J. Popat: Hodgkin Building, Kings College London, Guy's Campus
King Von R.: St Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary, University of London
Gavin S. Bennett: Hodgkin Building, Kings College London, Guy's Campus
Preena N. Patel: Hodgkin Building, Kings College London, Guy's Campus
James W. Fawcett: University of Cambridge
Stephen B. McMahon: Hodgkin Building, Kings College London, Guy's Campus

Nature, 2002, vol. 416, issue 6881, 636-640

Abstract: Abstract The inability of axons to regenerate after a spinal cord injury in the adult mammalian central nervous system (CNS) can lead to permanent paralysis. At sites of CNS injury, a glial scar develops, containing extracellular matrix molecules including chondroitin sulphate proteoglycans (CSPGs)1,2. CSPGs are inhibitory to axon growth in vitro3,4,5, and regenerating axons stop at CSPG-rich regions in vivo6. Removing CSPG glycosaminoglycan (GAG) chains attenuates CSPG inhibitory activity7,8,9,10. To test the functional effects of degrading chondroitin sulphate (CS)-GAG after spinal cord injury, we delivered chondroitinase ABC (ChABC) to the lesioned dorsal columns of adult rats. We show that intrathecal treatment with ChABC degraded CS-GAG at the injury site, upregulated a regeneration-associated protein in injured neurons, and promoted regeneration of both ascending sensory projections and descending corticospinal tract axons. ChABC treatment also restored post-synaptic activity below the lesion after electrical stimulation of corticospinal neurons, and promoted functional recovery of locomotor and proprioceptive behaviours. Our results demonstrate that CSPGs are important inhibitory molecules in vivo and suggest that their manipulation will be useful for treatment of human spinal injuries.

Date: 2002
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DOI: 10.1038/416636a

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