gms | German Medical Science

60th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Benelux countries and Bulgaria

German Society of Neurosurgery (DGNC)

24 - 27 May 2009, Münster

“Pain-related” cannabinoid CB1 receptor expression at the spinal and supra-spinal level after experimental spinal cord lesions in rats

Meeting Abstract

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

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocMO.13-02

doi: 10.3205/09dgnc090, urn:nbn:de:0183-09dgnc0904

Published: May 20, 2009

© 2009 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: To further investigate mechanisms underlying central neuropathic pain after spinal cord injury (SCI), we established the expression profiles of cannabinoid CB1 receptor immunoreactivity on spinal and supra-spinal levels after experimental SCI.

Methods: Spinal cord impact lesions (100kdyn, 200kdyn) were induced at the level of T9 by Infinite-Horizon-Impactor (PSI, Lexington, KY). Controls received a laminectomy. Mechanical and thermal allodynia were investigated for 6 weeks. Animals were sacrificed on day 7 and 42 after SCI. Expression of CB1 receptor was anatomically analyzed on serial sc and brain sections. Different lots of a highly selective antibody against the C-terminal 13 amino acids of CB1 were used (kindly provided by Professor M.R. Elphick, London). Quantification of CB1 receptor immunoreactivity (IR) was performed via ImageJ (1.37). Double labelling with GFAP, CD11b, ED-1, NF200/MAP-2, and nociceptive markers (CGRP, NK1 and TRPV1/TRPV1-P) were performed. Quantified CB1 receptor IR was correlated with behavioural data in respect to development of central neuropathic pain.

Results: The animals’ locomotor ability and development of chronic neuropathic pain correlated with the degree of injury. At the spinal cord level, the CB1 receptor IR was expressed at the lamina I to III of the dorsal horns and dorsolateral funiculus. Animals exhibiting chronic pain behaviour exhibited a significant induction of CB1 receptor IR in these regions at level L3 to L5 compared to sham and 100kdyn groups. This IR was co-localized with neuronal markers, CGRP, NK1, and TRPV1. At the supra-spinal levels, the CB1 receptor IR was expressed in olfactory-related structures, basal ganglia, associated structures, cortical layers (II–III), and hippocampal formation (stratum pyramidale CA3, molecular layer of dentate gyrus). In respect to the latter, there was significant down regulation of CB1 IR in animals exhibiting central pain behaviour.

Conclusions: Our data confirm that the CB1 receptor is involved at different anatomical levels and modes of central neuropathic pain processing. These findings provide an anatomical framework supporting further functional approaches to investigate novel mechanisms of central pain after SCI.