gms | German Medical Science

68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

Article

Send article

The effect of S100B on synaptogenesis and inflammatory processes in the hippocampus following experimental traumatic brain injury

Meeting Abstract

Search Medline for

  • Tina Sehm - Universitätsklinikum Erlangen, Klinik für Neurochirurgie, Erlangen, Deutschland
  • Justus Baecker - Universitätsklinikum Erlangen, Klinik für Neurochirurgie, Erlangen, Deutschland
  • Ali Ghoochani - Universitätsklinikum Erlangen, Klinik für Neurochirurgie, Erlangen, Deutschland
  • Michael Buchfelder - Universitätsklinikum Erlangen, Klinik für Neurochirurgie, Erlangen, Deutschland
  • Andrea Kleindienst - Universitätsklinikum Erlangen, Klinik für Neurochirurgie, Erlangen, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocMi.20.04

doi: 10.3205/17dgnc502, urn:nbn:de:0183-17dgnc5025

Published: June 9, 2017

© 2017 Sehm et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: : The stimulated release of the neurotrophic protein S100B is known to enhance hippocampal progenitor cell proliferation, neuronal differentiation and cognitive recovery following traumatic brain injury (TBI). However, the effect of S100B on synaptogenesis and inflammatory has not been elucidated yet. In the present study, we investigate the effect of S100B on the microglial activation n and the synaptic density in the hippocampus following experimental TBI.

Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion or sham injury, and S100B (50ng/hr) or PBS was infused into the lateral ventricle for 7 days using osmotic micro-pumps. The animals were sacrificed on day 5 or 34 post-injury, and 5µm sections (distance 100µm, bregma -3.3 to -5.6mm) were analyzed histologically. The hippocampal microglial activation and synaptic density were quantified by immunostaining applying marker against CD68 (ED1) – a single chain membrane bound glycoprotein and synaptophysin (SYN) – a synaptic vesicle glycoproteine.

Results: S100B attenuated bilateral the SYN expression in the hippocampus (week 5: CA1 region, p<0.001; CA3 region, p≤0.001; GCL, p<0.001) both in uninjured animals and following TBI. This effect was present on day 5 and after 5 weeks. The stimulated CD68 expression displayed a similar spatial profile (week 5: CA3 region, p=0.008; GCL, p<0.001).

Conclusion: Our results demonstrate that S100B attenuates the hippocampal SYN expression and induces a microglial activation in non-injured and in injured animals. This effect is not limited to the lesion side, but also comprises a long-term effect in the contralateral hemisphere. Whether the reduction of synaptic density is directly caused by S100B or is mediated through the triggered neuroinflammatory response remains unclear. However, since we demonstrated earlier in the same animals that S100B augments significantly hippocampal neurogenesis and improves cognitive function, the S100B induced microglial activation does not counteract neuroregeneration within the first five weeks post-injury. Further studies are required to elucidate the respective cellular signalling and possible long-term effects.