Journal article

Invasion of lesion territory by regenerating fibers after spinal cord injury in adult macaque monkeys

  • Beaud, Marie-Laure Department of Medicine and Program in Neurosciences, Faculty of Sciences and Fribourg Center for Cognition, University of Fribourg, Switzerland
  • Rouiller, Eric M. Department of Medicine and Program in Neurosciences, Faculty of Sciences and Fribourg Center for Cognition, University of Fribourg, Switzerland
  • Bloch, Jocelyne Department of Neurosurgery, Neurosurgery Clinic, University Hospital of Lausanne, Switzerland
  • Mir, Anis Neuroscience Research, Novartis Institute for BioMedical Research, Basel, Switzerland
  • Schwab, M.E. Brain Research Institute, Department of Neuromorphology, University and ETH Zurich, Switzerland
  • Wannier, Thierry Department of Medicine and Program in Neurosciences, Faculty of Sciences and Fribourg Center for Cognition, University of Fribourg, Switzerland - Brain Research Institute, Department of Neuromorphology, University and ETH Zurich, Switzerland
  • Schmidlin, Eric Department of Medicine and Program in Neurosciences, Faculty of Sciences and Fribourg Center for Cognition, University of Fribourg, Switzerland
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    2012
Published in:
  • Neuroscience. - 2012, vol. 27, p. 271–282
English In adult macaque monkeys subjected to an incomplete spinal cord injury (SCI), corticospinal (CS) fibers are rarely observed to grow in the lesion territory. This situation is little affected by the application of an anti-Nogo-A antibody which otherwise fosters the growth of CS fibers rostrally and caudally to the lesion. However, when using the Sternberger monoclonal-incorporated antibody 32 (SMI-32), a marker detecting a non-phosphorylated neurofilament epitope, numerous SMI-32-positive (+) fibers were observed in the spinal lesion territory of 18 adult macaque monkeys; eight of these animals had received a control antibody infusion intrathecally for 1 month after the injury, five animals an anti-Nogo-A antibody, and five animals received an anti-Nogo-A antibody together with brain-derived neurotrophic factor (BDNF). These fibers occupied the whole dorso-ventral axis of the lesion site with a tendency to accumulate on the ventral side, and their trajectories were erratic. Most of these fibers (about 87%) were larger than 1.3 μm and densely SMI-32 (+) stained. In the undamaged spinal tissue, motoneurons form the only large population of SMI-32 (+) neurons which are densely stained and have large diameter axons. These data therefore suggest that a sizeable proportion of the fibers seen in the lesion territory originate from motoneurons, although fibers of other origins could also contribute. Neither the presence of the antibody neutralizing Nogo-A alone, nor the presence of the antibody neutralizing Nogo-A combined with BDNF influenced the number or the length of the SMI-32 (+) fibers in the spinal lesion area. In summary, our data show that after a spinal cord lesion in adult monkeys, the lesion site is colonized by fibers, a large portion of which presumably originate from motoneurons.
Faculty
Faculté des sciences et de médecine
Department
Département de Médecine
Language
  • English
Classification
Biology
License
License undefined
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Persistent URL
https://folia.unifr.ch/unifr/documents/302691
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