gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Article

Send article

Chemokine expression and development of central pain syndromes after spinal cord injury in the rat

Chemokinexpression und Entwicklung zentraler Schmerzen nach spinalem Trauma in der Ratte

Meeting Abstract

Search Medline for

  • corresponding author F. Knerlich - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel
  • M. Juraschek - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel
  • H. M. Mehdorn - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel
  • J. Held-Feindt - Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocSA.07.09

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2007/07dgnc183.shtml

Published: April 11, 2007

© 2007 Knerlich et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

Objective: Spinal cord injury (SCI) is often associated with development of chronic pain syndromes. Using a force defined SCI model for rats lesions of 3 different severity grades were induced. They were investigated for mechanical and thermal allodynia through a 6 week survival time course. Spinal cord expression of CCL2/CCR2 and CCL3/CCR1 was analyzed 7d, 15d, and 42d after lesion.

Methods: Long Evans rats (n=57) were used. They received laminectomy on T8. A 1N, 1.5N, or 2N impact was applied with the Infinite-Horizon-Impactor device (PSI, Lexington, KY). Controls received laminectomy without impact injury (n=13). Animals were tested for mechanical and thermal allodynia and sacrificed 7d (n=15), 15d (n=15), and 42d (n=14) after SCI. Immunohistochemistry (IHC) and real time PCR (RT-PCR) was performed for CCL2/CCR-3 and CCL3/CCR1. Double IHC with cell markers for astrocytes (GFAP), microglia (CD11b/OX-42), monocytes /macrophages (ED-1), neurons (NeuN), CGRP, and TLR4 was done.

Results: The development of mechanical and thermal allodynia significantly correlated with the degree of injury. CCL2 and CCL3 mRNA was up regulated force and time dependent after injury. In the early time course CCL2 ir co-localized with GFAP and TLR4 in the lesion rim. In contrast, 42d after lesion there was additionally strong CCL2 ir seen in astroglial cells in the dorsal horns and dorsal columns of severely injured animals. CCL3 was expressed in the lesion by inflammatory cells at DPO 15 and 42. The CCR2 receptor mRNA was induced after 7d. The CCR2 ir was seen in the dorsal horns at lesion level in all groups. The ir co-localized partially with CGRP. At later timepoints, CCR2 ir was seen at lesion level in astrocytic cells. In contrast, CCR1 mRNA and ir was strongly induced at the later survival time points. There was a strong glial CCR1 ir at lesion level. At DPO 42 the CCR1 ir was expressed in the dorsal columns of severely injured animals.

Conclusions: The investigated chemokines and their receptors showed an individual expression pattern on mRNA and ir level. The strong induction of CCL2 and CCR1 in the dorsal columns and dorsal horn may play a role in the development of chronic central pain syndromes after severe SCI.