gms | German Medical Science

59th Annual Meeting of the German Society of Neurosurgery (DGNC)
3rd Joint Meeting with the Italian Neurosurgical Society (SINch)

German Society of Neurosurgery (DGNC)

1 - 4 June 2008, Würzburg

Time dependent changes in the spinal cord white matter precursor niche: Radial glia expression of chemokines after traumatic spinal cord injury in adult rats

Chemokinexpression in radialer Glia nach traumatischer Rückenmarksläsion in adulten Ratten

Meeting Abstract

  • corresponding author F. Knerlich-Lukoschus - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel
  • B. v. d. Ropp-Brenner - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel
  • H. M. Mehdorn - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel
  • J. Held-Feindt - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel

Deutsche Gesellschaft für Neurochirurgie. Società Italiana di Neurochirurgia. 59. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3. Joint Meeting mit der Italienischen Gesellschaft für Neurochirurgie (SINch). Würzburg, 01.-04.06.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocP 066

The electronic version of this article is the complete one and can be found online at:

Published: May 30, 2008

© 2008 Knerlich-Lukoschus et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Endogenous neural stem cells and precursor cells are a promising therapeutical option for spinal cord injury. Factors that determine their proliferation and differentiation abilities in adult mammals under pathological conditions have to be investigated. In this study, expression of crucial chemokines and their receptors was investigated at different survival time points after spinal cord impact lesion.

Methods: Adult male Long Evans rats received laminectomy on T8, were mounted in the Infinite-Horizon-Impactor device, and 1N or 2N impact was applied. Controls received laminectomy without impact injury (n=10). Locomotor ability was assessed via BBB open field test. Rats were sacrificed 48h (n=5), 7d (n=5), 15d (n=5), and 42d (n=5) after SCI. Immunohistochemistry (IHC) and real time PCR (RT-PCR) was performed for CCL2/CCR2, CCL3/CCR1, SDF/CXCR4, and CX3CL1/CX3CR1. Double IHC with cell markers for astrocytes (GFAP), microglia (CD11b/OX-42), monocytes /macrophages (ED-1) and neurons (MAP-2, NF150) was performed. For detecting early developed cells, Nestin was stained. BLBP and 2CB3 were used as radial glial markers. As proliferation marker BrdU labelling was performed on some animals co-stained with Nestin, BLBP, and chemokines.

Results: CCL2 and CCL3 mRNA was up-regulated force and time dependent after lesion: At later time points (15 and 42 days) the mRNA expression was stronger induced in the 2N- compared to the 1N-treatment group. CCL2 and CCL3 immunoreactivity (ir) was seen in round inflammatory cells in the lesion in all three treatment groups at post operative day (DPO) 2 and 7. In contrast, at DPO 15 and 42 there was a strong CCL2 ir seen in glial cells not only in the lesion rim, but also in thoracic with matter and dorsal columns. SDF and CX3CL1 were induced on mRNA and ir level in severely injured animals at DPO 7 and 15 on lesion level. The chemokine receptors CCR1, CXCR4 were strongly induced in the subpial white matter and dorsal columns of severely injured animals, more pronounced in the later survival time points. This ir, and CCL3 and CCL2 ir was co-localized and partially co-expressed with 2CB3, BLBP and Nestin. In those white matter inflammatory foci, Nestin positive BrdU labeled cells were tightly co-localized with chemokine immunoreactive radial glial cells.

Conclusions: To conclude strong and time-dependent expression of chemokines in subpial white matter radial glia is co-localized with proliferating cells and precursor markers.