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

Differential expression of calcium-binding proteins in spinal cord after experimental spinal cord compression

Meeting Abstract

  • M. Setzer - H. Lee Moffitt Cancer Center and Research Institute, Neurooncology Program, University of South Florida, College of Medicine, Tampa, Florida, USA
  • F. Vrionis - H. Lee Moffitt Cancer Center and Research Institute, Neurooncology Program, University of South Florida, College of Medicine, Tampa, Florida, USA
  • N. Ulfig - Neuroembryologisches Forschungslabor, Institut für Anatomie, Universität Rostock
  • V. Seifert - Klinik für Neurochirurgie, Johann-Wolfgang-Goethe-Universität, Frankfurt am Main
  • G. Marquardt - Klinik für Neurochirurgie, Johann-Wolfgang-Goethe-Universität, Frankfurt am Main

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. DocP11-10

doi: 10.3205/09dgnc373, urn:nbn:de:0183-09dgnc3730

Published: May 20, 2009

© 2009 Setzer 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: The calcium binding proteins parvalbumin, calbindin and calretinin which are members of the EF hand family, are cytoplasmic proteins with the capability of buffering excessive intracellular calcium influx which results into a neuroprotective effect. The aim of the present study was to examine the expression of parvalbumin, calbindin and calretinin in the rabbit thoracic spinal cord after experimental compression.

Methods: A rabbit model of spinal cord compression was used which allows for a gradual 270° compression of the spinal cord (experimental group n=25, control group n=5). Once neurological deficits had developed the spinal cord was decompressed by removal of the compressing silicone band. Spinal cords were perfusion-fixed with 4% paraformaldehyde and epicenters were removed, stained immunohistochemically (single and double labeling techniques) with antibodies against parvalbumin, calbindin and calretinin, and analyzed with light and confocal laser microscopy. Clinical outcome variables and histological results were correlated and differences in outcome groups compared.

Results: In normal rabbit spinal cord calretinin and parvalbumin were colocalized in ventral horn alpha‑motoneurons as well as in smaller dorsal and ventral horn interneurons. Calbindin showed a complementary distribution pattern with intense staining of substantia gelatinosa neurons and neuropil. Alpha-motoneurons did not show any calbindin immunoreactivity. Double labeling with anti-calbindin and anti-GFAP showed colocalization of both proteins in a group of subpial astroglial cells. After spinal cord compression some of the alpha-motoneurons expressed calbindin especially in animals with severe neurological deficits and a good recovery. Animals with no recovery and a permanent deficit did not show calbindin-positive motoneurons.

Conclusions: The protein expression patterns change significantly between outcome groups with de novo expression of calbindin in ventral horn motorneurons in instances of good recovery after spinal cord compression. This suggests a neuroprotective role of calbindin in subacute and chronic spinal cord compression.