Chronically injured corticospinal axons do not cross large spinal lesion gaps after a multifactorial transplantation strategy using olfactory ensheathing cell/olfactory nerve fibroblast-biomatrix bridges
English
Deumens, R.[European Graduate School of Neuroscience (EURON), University of Maastricht, The Netherlands > Department of Psychiatry and Neuropsychology > Division Neuroscience > >]
Koopmans, G. C.[Academic Hospital Maastricht and European Graduate School of Neuroscience (EURON), University of Maastricht, The Netherlands > Department of Anesthesiology (Academic Hospital) and Department of Psychiatry and Neuropsychology (University of Maastricht) > > >]
Honig, W. M. M.[Academic Hospital Maastricht, Maastricht, The Netherlands > Department of Anesthesiology > > >]
Maquet, Véronique[University of Liège (ULg) > Department of Chemistry > Center for Education and Research on Macromolecules (CERM) > >]
Jérôme, Robert[University of Liège (ULg) > Department of Chemistry > Center for Education and Research on Macromolecules (CERM) > >]
Steinbusch, H. W. M.[European Graduate School of Neuroscience (EURON), University of Maastricht, The Netherlands > Department of Psychiatry and Neuropsychology > Division Neuroscience > >]
Joosten, E. A. J.[Academic Hospital Maastricht, Maastricht, The Netherlands > Department of Anesthesiology > > >]
[en] Transplantation of mixed cultures containing olfactory ensheathing cell (OEC) and olfactory nerve fibroblasts (ONF) has been shown to stimulate regrowth of both acutely and chronically injured corticospinal (CS) axons across small spinal cord lesion gaps. Here, we used a multifactorial transplantation strategy to stimulate regrowth of chronically injured CS axons across large spinal cord lesion gaps. This strategy combined the transplantation of aligned OEC/ONF-biomatrix complexes, as described previously (Deumens et al. [2004] Neuroscience 125:591-604), within the lesion gap with additional OEC/ONF injections rostral and caudal to the lesion site. We show an enhanced presence of injured CS axons directly rostral to the lesion gap, with no effects on injured CS axons at or caudal to the lesion gap. Furthermore, injured CS axons did not penetrate the OEC/ONF-biomatrix complex within the lesion gap. The enhanced presence of CS axons rostral to the lesion gap was not accompanied by any recovery of behavioral parameters assessed with the BBB locomotor rating scale or CatWalk gait analysis. We conclude that our multifactorial transplantation strategy should be optimized to create an OEC/ONF continuum in the injured spinal cord and thereby stimulate regrowth of injured CS axons across large spinal lesion gaps.
Center for Education and Research on Macromolecules (CERM)