gms | German Medical Science

64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

Activation of brain residential microglia is responsible for delayed neuronal apoptosis after experimental subarachnoid hemorrhage

Meeting Abstract

  • Ulf C. Schneider - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Anja-Maria Radon - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Salima Magrini - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Etienne N. Atangana - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Frank Heppner - Institut für Neuropathologie, Charité – Universitätsmedizin Berlin
  • Peter Vajkoczy - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocMO.09.05

doi: 10.3205/13dgnc075, urn:nbn:de:0183-13dgnc0757

Published: May 21, 2013

© 2013 Schneider 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: Inflammatory mechanisms have become an interesting target for analysis of early and delayed brain injury after subarachnoid hemorrhage (SAH). Our group could demonstrate a microglia activation in the central nervous system (CNS) after SAH, which peaks 7-14 days after the bleeding. To evaluate a relationship of microglia activation with neuronal injury, a microglia-depletion mouse model was applied.

Method: Mice harbouring a Herpes simplex virus thymidine kinase (HSVTK) underwent intraventricular implantation of an osmotic minipump filled with ganciclovir (GCV) for microglia depletion in the CNS. Experimental SAH was induced through endovascular perforation. Wildtype mice and sham operated animals (with and without GCV pump) served as controls. Neuronal injury was evaluated in frozen brain sections using a NeuN/TUNEL Kit co-staining and counting of apoptoses in serial sections.

Results: A marked increase of neuronal apoptosis was documented on day 7 and 14 after SAH in wildtype animals compared to sham animals (without GCV pump) (day7: 212 ± 125 vs. 98 ± 19; day14: 273 ± 127 vs. 63 ± 21 (counts per brain slice)). In HSVTK-/- mice (with GCV pump) 219 ± 52 apoptoses were counted on day 7, while in HSTTK+/+ mice (with GCV pump), only 61 ± 15 apoptoses were seen (p < .01)

Conclusions: The activation of brain residential microglia cells parallels neuronal apoptosis after subarachnoid hemorrhage. The depletion of microglia leads to a significant reduction of neuronal apoptosis. These results show, that inflammatory microglia activation within the CNS parenchyma contributes to secondary brain injury after SAH.