gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

Nestin-expressing cells adopt a complex electrophysiological phenotype following mild ischemic episode

Nestin positive Zellen erwerben einen komplex elektrophysiologischen Phänotyp nach milder ischämischer Episode

Meeting Abstract

  • corresponding author M. Synowitz - Department of Neurosurgery, Helios Hospital Berlin, Berlin
  • G. Kronenberg - Volkswagen Stiftung Research Group, Department of Experimental Neurology, Charité University Hospital, Humboldt University, Berlin
  • L. P. Wang - Cellular Neuroscience Group, Max Delbrück Centre for Molecular Medicine (MDC), Berlin
  • K. Gertz - Volkswagen Stiftung Research Group, Department of Experimental Neurology, Charité University Hospital, Humboldt University, Berlin
  • J. Katchanov - Volkswagen Stiftung Research Group, Department of Experimental Neurology, Charité University Hospital, Humboldt University, Berlin
  • C. Harms - Department of Neurology, Charité University Hospital, Humboldt University, Berlin
  • R. Glass - Cellular Neuroscience Group, Max Delbrück Centre for Molecular Medicine (MDC), Berlin
  • G. Kempermann - Volkswagen Stiftung Research Group, Department of Experimental Neurology, Charité University Hospital, Humboldt University, Berlin
  • H. Kettenmann - Cellular Neuroscience Group, Max Delbrück Centre for Molecular Medicine (MDC), Berlin
  • M. Endres - Department of Neurology, Charité University Hospital, Humboldt University, Berlin

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. DocP079

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Veröffentlicht: 4. Mai 2005

© 2005 Synowitz 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

The intermediate filament nestin is upregulated in response to cerebral ischemia, the significance of this, however, is incompletely understood. The present study was designed to describe in a comprehensive immunohistochemical and electrophysiological approach the effects of mild transient ischemia on nestin-expressing cells in the striatum up to 8 weeks following occlusion and reperfusion of MCA.

Methods

Here, we used transgenic mice that express green fluorescent protein (GFP) under control of the nestin promotor to characterize the fate of nestin-expressing cells up to 8 weeks following 30 min occlusion of the middle cerebral artery (MCAo) and reperfusion. Immunofluorescent triple labeling was carried out on 40-μm-free-floating sections using a spectral confocal microscope.

Results

The population of nestin-GFP+ cells increased in the ischemic lesion rim and core within 4 days, did not become TUNEL-positive and were detectable up to 8 weeks in the lesion scar. Nestin-GFP+ cells proliferated in situ and underwent approximately one round of cell division. They were not recruited in large numbers from the subventricular zone (SVZ) as indicated by absence of co-labeling with intracerebroventricularly injected dye DiI in the majority of nestin-GFP+ cells and absence of migration chains. Nestin-GFP+ cells expressed the chondroitin sulfate proteoglycan NG2 and nestin protein, but typically lacked astrocytic markers, i.e. glial fibrillary acid protein (GFAP) or S100ß. Vice versa, the majority of GFAP+ cells lacked nestin-expression and surrounded the ischemic lesion by 4 days. Whole cell patch clamp recordings in acute brain slices from controls demonstrated that about half of the cells had complex membrane properties and expressed AMPA receptors but lacked glutamate transporters similar to progenitor cells and a newly described subpopulation of astrocytes. 4 days after the insult all nestin-GFP+ cells expressed these properties.

Conclusions

We hypothesize that the change in physiological properties induced by the ischemic insult is directed toward a network function and early neuronal differentiation of nestin-expressing cells.