gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

The neurotrophic protein S100B enhances hippocampal neurogenesis following a unilateral parietal brain lesion in mice

Meeting Abstract

  • A. Kleindienst - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • F. Grünbeck - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • I. Emtmann - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • K. Eck - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • M. Buchfelder - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg

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. DocP09-06

doi: 10.3205/09dgnc346, urn:nbn:de:0183-09dgnc3463

Veröffentlicht: 20. Mai 2009

© 2009 Kleindienst 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 vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: While elevated serum S100B levels are correlated to poor outcome after traumatic brain injury, experimental data on the other hand, demonstrate a neuroprotective and neurotrophic effect of this calcium-binding protein. The purpose of this study was to examine the effect of S100B treatment following experimental brain injury.

Methods: Juvenile (4 week old) male mice were subjected to a discrete unilateral parietal cryolesion or sham procedure. They were treated with vehicle or S100B given intra-peritoneally once daily at 20nM or 200nM for either 4 or 14 days (n=4 each group). Cell proliferation was assessed by injecting the mitotic marker bromodeoxyuridine (BrdU) for either 4 or 14 days. Animals were sacrificed on day 4 or 28, and the brains were paraffin-embedded. Immunostaining with anti-BrdU was done on 5μm sections each 100μm apart throughout the hippocampus. Differentiation of the proliferating cells was examined by triple-labeling with the neuronal marker NeuN or the glial marker GFAP. Statistical analysis was performed by an analysis of variance, and significance was accepted at p<0.05.

Results: There were no differences in cell counts between the ipsi- and contralateral dentate gyrus. Quantification of BrdU-immunoreactive cells revealed a S100B-enhanced progenitor cell proliferation in a dose-dependent manner as assessed in the subgranular zone on day 4 (p=0.019). Furthermore, S100B augmented the survival of these cells as quantified on day 28 (p=0.002). S100B promoted the neuronal differentiation by 30%. Assessment of S100B in serum (Elecsys®, Roche Diagnostics, measuring range 0.005-39µg/l) did not reveal any significant differences at the end of the experiments.

Conclusions: Our findings indicate that an intra-peritoneal treatment with S100B induces progenitor cell proliferation within the germinative area of the hippocampus, the subsequent survival of these cells as well as their differentiation into neurons. These observations provide compelling evidence for the therapeutic potential of S100B following brain injury.