Nature Neuroscience
7, 269 - 277 (2004)
Published online: 15 February 2004; | doi:10.1038/nn1195
The injured spinal cord spontaneously forms a new intraspinal circuit in adult ratsFlorence M Bareyre1, 2, Martin Kerschensteiner1, 2, Olivier Raineteau3, Thomas C Mettenleiter4, Oliver Weinmann1
& Martin E Schwab11
Department of Neuromorphology, Brain Research Institute, University of Zürich and Department of Biology, ETH Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland. 2
Present address: Department of Anatomy and Neurobiology, Washington University School of Medicine, 660 South Euclid, Box 8108, St. Louis, Missouri 68110, USA. 3
Department of Neurophysiology, Brain Research Institute, University of Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland. 4
Institute of Molecular and Cellular Virology, Friedrich-Loeffler-Institute, Federal Research Center for Virus Diseases of Animals, D-17498 Insel Riems, Germany.
Correspondence should be addressed to Florence M Bareyre florence@pcg.wustl.eduIn contrast to peripheral nerves, central axons do not regenerate. Partial injuries to the spinal cord, however, are followed by functional recovery. We investigated the anatomical basis of this recovery and found that after incomplete spinal cord injury in rats, transected hindlimb corticospinal tract (CST) axons sprouted into the cervical gray matter to contact short and long propriospinal neurons (PSNs). Over 12 weeks, contacts with long PSNs that bridged the lesion were maintained, whereas contacts with short PSNs that did not bridge the lesion were lost. In turn, long PSNs arborize on lumbar motor neurons, creating a new intraspinal circuit relaying cortical input to its original spinal targets. We confirmed the functionality of this circuit by electrophysiological and behavioral testing before and after CST re-lesion. Retrograde transynaptic tracing confirmed its integrity, and revealed changes of cortical representation. Hence, after incomplete spinal cord injury, spontaneous extensive remodeling occurs, based on axonal sprout formation and removal. Such remodeling may be crucial for rehabilitation in humans.
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