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Brain Advance Access originally published online on April 16, 2009
Brain 2009 132(6):1426-1440; doi:10.1093/brain/awp085
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© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Differential effects of anti-Nogo-A antibody treatment and treadmill training in rats with incomplete spinal cord injury

Irin C. Maier1,2,*, Ronaldo M. Ichiyama3,4,*, Grégoire Courtine4,5,*, Lisa Schnell1,2, Igor Lavrov4, V. Reggie Edgerton4,6,7 and Martin E. Schwab1,2

1 Brain Research Institute, University of Zurich, Zurich, Switzerland 2 Department of Biology, Swiss Federal Institute of Technology, 8057 Zurich, Switzerland 3 Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK 4 Department of Physiological Science, University of California, Los Angeles, CA, USA 5 Experimental Neurorehabilitation Laboratory, University of Zurich, Zurich, Switzerland 6 Department of Neurobiology, University of California, Los Angeles, CA, USA 7 Brain Research Institute, University of California, Los Angeles, California 90095, USA

Correspondence to: Irin Maier, Brain Research Institute, Winterthurerstrasse 190, 8057 Zurich, Switzerland E-mail: imaier{at}hifo.uzh.ch

Locomotor training on treadmills can improve recovery of stepping in spinal cord injured animals and patients. Likewise, lesioned rats treated with antibodies against the myelin associated neurite growth inhibitory protein, Nogo-A, showed increased regeneration, neuronal reorganization and behavioural improvements. A detailed kinematic analysis showed that the hindlimb kinematic patterns that developed in anti-Nogo-A antibody treated versus treadmill trained spinal cord injured rats were significantly different. The synchronous combined treatment group did not show synergistic effects. This lack of synergistic effects could not be explained by an increase in pain perception, sprouting of calcitonin gene-related peptide (CGRP) positive fibres or by interference of locomotor training with anti-Nogo-A antibody induced regeneration and sprouting of descending fibre tracts. The differential mechanisms leading to behavioural recovery during task-specific training and in regeneration or plasticity enhancing therapies have to be taken into account in designing combinatorial therapies so that their potential positive interactive effects can be fully expressed.

Key Words: spinal cord injury; locomotor training; Nogo-A; neuronal plasticity and regeneration; functional recovery

Abbreviations: BDA, biotindextrane amine; CGRP, calcitonin gene-related peptide; CNS, central nervous system; CST, corticospinal tract; PCA, principal component analysis; SCI, spinal cord injury

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Received September 25, 2008. Revised February 24, 2009. Accepted February 25, 2009.

*These authors contributed equally to this work.


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