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

The neurotrophic protein S100B enhances the injury-induced astrocytosis in the germinative area of the hippocampus

Das neurotrophe Protein S100B stimuliert die Trauma-induzierte Astrozytose in der germinativen Zone des Hippokampus

Meeting Abstract

  • corresponding author Q. Zhaohua - Institut für Neuropathologie, Universitätsklinikum Göttingen, Deutschland
  • F. Hesse - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg, Erlangen, Deutschland
  • C. Stadelmann - Institut für Neuropathologie, Universitätsklinikum Göttingen, Deutschland
  • M. Buchfelder - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg, Erlangen, Deutschland
  • A. Kleindienst - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg, Erlangen, Deutschland

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. DocFR.02.09

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2007/07dgnc074.shtml

Veröffentlicht: 11. April 2007

© 2007 Zhaohua et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: S100B has been promoted as a clinical marker of brain damage and high serum levels were considered to correlate with the severity of injury and a poor prognosis. However, experimental research demonstrated increased cerebral levels of the neurotrophic protein S100B to enhance hippocampal neurogenesis and to improve cognitive recovery following traumatic brain injury (TBI). The purpose of the present study was to elucidate the cellular effects of S100B.

Methods: Following lateral fluid percussion injury in male rats (n=32), we infused S100B (50ng/hr) or vehicle into the lateral ventricle for 7 days using an osmotic micro-pump. The animals were sacrificed on day 5 or 5 weeks post-injury, and 5um sections, 100um apart (bregma -3.3 to -5.6mm) were analysed histologically. Cell death was assessed using TUNEL and hematoxylin-eosin staining, gliosis was assessed by applying the glial markers GFAP and S100B, and axonal damage by APP immunostaining.

Results: TUNEL-positive cells were present directly beneath the lesion site in vehicle and S100B-infused animals on day 5 (238±6 and 234±24/mm2, respectively, n.s.), but not 5 weeks after TBI or in control animals. Following an intraventricular S100B infusion and TBI, we found an early increase of S100B expressing cells in the subcortical area (p=0.038) as well as a delayed stimulation of S100B expression within the area of the hippocampus dedicated to neurogenesis (p=0.041). Both, injury and S100B infusion in normal animals resulted in an increased number of GFAP expressing cells in the subcortical area (p=0.049) as well as in a decrease of those cells in the CA3 region (p=0.012) and hilus (p<0.001) of the hippocampus after 5 weeks. The intraventricular S100B infusion did not affect axonal injury following TBI, but resulted in an early (p=0.034) and prolonged (p=0.039) APP expression at the injury site.

Conclusions: In our model, the exogenous application of S100B did not exert an effect on early cell death or axonal injury. The significance of the delayed APP accumulation following injury has to be clarified by long-term experiments in order to exclude any participation in neurodegenerative processes. The stimulation of S100B expression in the germinative area of the hippocampus is in line with a participation of S100B in neurogenesis.