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61st Annual Meeting of the German Society of Neurosurgery (DGNC) as part of the Neurowoche 2010
Joint Meeting with the Brazilian Society of Neurosurgery on the 20 September 2010

German Society of Neurosurgery (DGNC)

21 - 25 September 2010, Mannheim

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Experimental spinal cord injury (SCI): chemokine and cannabinoid CB1 receptor expression patterns in correlation with neuropathic pain development

Meeting Abstract

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  • Friederike Knerlich-Lukoschus - Neurochirurgische Klinik, UK SH, Campus Kiel, Germany
  • B. v.d. Ropp-Brenner - Neurochirurgische Klinik, UK SH, Campus Kiel, Germany
  • R. Lucius - Anatomisches Institut der CAU, Kiel, Germany
  • H. Maximilian Mehdorn - Neurochirurgische Klinik, UK SH, Campus Kiel, Germany
  • Janka Held-Feindt - Neurochirurgische Klinik, UK SH, Campus Kiel, Germany

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocP1865

doi: 10.3205/10dgnc336, urn:nbn:de:0183-10dgnc3368

Published: September 16, 2010

© 2010 Knerlich-Lukoschus 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

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Objective: Involvement in neuro-modulatory processes makes the endogenous cannabinoid/chemokine system a potential key element in cascades underlying central neuropathic pain development after SCI. Therefore, detailed expression profiles of chemokines, their receptors and cannabinoid CB1 receptor were investigated in an experimental rat SCI paradigm.

Methods: Thoracic spinal cord (sc) impact lesions (100kdyn, 200kdyn) were induced by Infinite-Horizon-Impactor (PSI, Lexington, KY). Controls received laminectomy. Mechanical and thermal allodynia were investigated for 6 weeks. Rats were sacrificed on day 3, 7, 14 and 42 after SCI. Expression of CCL3/CCR1, SDF-1α/CXCR4, CB1 receptor were analyzed by real-time RT-PCR, immunohistochemistry (IHC) and densitometry. Commercial chemokine antibodies and a highly selective antibody against CB1 C-terminal were used (Professor M.R. Elphick, London). Double labelling with cellular and nociceptive markers (Substance-P, CGRP, NK1, TRPV1/TRPV1-P, TRPV2) was performed. IHC densities were correlated with behavioural data.

Results: CCL3/CCR1 were induced early in dorsal horns (DH) (lamina I and II) and dorsal columns (DC), increasing on high levels up to day 42 esp. after 200kdyn lesions. SDF-1α/CXCR4 were induced more widespread throughout the DH, continuously increasing up to day 42 after 100kdyn and 200kdyn lesion. There was constitutive CB1 receptor expression in DH lamina I to III and dorsolateral funiculus, which was induced in the late time-course after SCI. Additionally CB1 receptor was induced in DC after SCI. CCL3/CCR1 were co-expressed with TRPV1/TRPV1P in DH, and TRPV2 in DC; CB1 receptor was co-localized with all nociceptive markers. CCL3/CCR1 and CB1 receptor IHC-densities correlated significantly with central pain related behaviour.

Conclusions: Chemokines/-receptors and CB1 receptor exhibited individual time-dependent expression patterns in pain relevant sc regions, correlating partially with chronic pain development. These findings provide an anatomical framework supporting functional approaches to further crucial mechanisms of central pain after SCI.