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Projects - Role of neutrophil granulocytes and microglia in ischemic tissue damage in the CNS - Leibniz Institute for Neurobiology, Magdeburg
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 Projects

 Role of neutrophil granulocytes and microglia in ischemic tissue damage in the CNS

Principle investigators: Monika Riek-Burchardt,
Jens Neumann ( )

Global ischemia (in vivo)
In our study the main interest focussed on the influence of ischemia on activation and proliferation of microglia cells in the rat forebrain shortly (3 days) after global ischemia (transient two-vessel occlusion combined with hypotension). Evaluations were performed in the dorsal hippocampus, where post-ischemic cell death develops selectively in the CA1 area, and in distant areas like the ventricle wall and the striatum. Immunfluorescence together with confocal laser microscopy was used to identify proliferation (BrdU incorporation in the DNA during cell replication). In the global ischemia model, proliferation (BrdU+) significantly increased throughout the forebrain (hippocampus, striatum, ventricle wall) three days after ischemia The vast majority of newly generated cells were activated microglia/macrophages, which invaded in morphologically damaged as well as undamaged areas.

In conclusion, during the first days after global ischemia, cell death of CA1-neurons was accompanied by a massive overall proliferation and activation of microglia cells and macrophages.

(A-D) expression of microglia/macrophages in the hippocampus following global ischemia after 3 days in vivo. (A) Z-stack of a newly generated cell positive for both BrdU and OX-42, (B) two separated channels and the merged picture are presented to demonstrate the double-labelled cells. (C, D) double-labelling (arrows) for BrdU (green) and OX-42 (red) in the CA1 region. But there are also many microglia/macrophages which are not newly born after ischemia (asterisk).

(A-D) expression of microglia/macrophages in the hippocampus following global ischemia after 3 days in vivo. (A) Z-stack of a newly generated cell positive for both BrdU and OX-42, (B) two separated channels and the merged picture are presented to demonstrate the double-labelled cells. (C, D) double-labelling (arrows) for BrdU (green) and OX-42 (red) in the CA1 region. But there are also many microglia/macrophages which are not newly born after ischemia (asterisk).

Oxygen glucose deprivation (in vitro)
Our aim was to identify the role of microglia in the early phase of the cerebral ischemic insult. We have established a model, where we applied exogenous fluorescence-labelled BV-2 microglia directly onto an organotypic hippocampal slice culture after oxygen glucose deprivation (OGD). With this model we are able to investigate exclusively the role of microglia by excluding the in vivo participating infiltrating blood cells (granulocytes, monocytes etc.). Further, with this model we can reach pathophysiological relevant numbers of microglia in our system and we can simulate the migration of microglia from other brain regions towards the site of injury. Neuronal cell death after oxygen-glucose deprivation (OGD) was determined by PI incorporation and Nissl staining. Migration and interaction with neurons was analysed by time resolved three-dimensional 2-photon microscopy. Using a transgenic mice, witch expresses eYFP in a subset of neurons and fluorescently labelled microglia, a migration of microglia into the slice and a close cell-cell interaction with the neurons after was observed in the slice. This microglia application protects against OGD-induced neuronal damage even when applied up to 4h after OGD (Neumann et al., 2005). The induction of migration and neuron-microglia interaction deep inside the slice was markedly increased under OGD conditions. In acute injury such as trauma or stroke appropriately activated microglia may primarily have a neuroprotective role. Thus, anti-inflammatory treatment within the protective time window of microglia would therefore be counterintuitive.

Bei der externen Zugabe von Mikrogliazellen bis zu 4 Stunden nach einem Insult, wirken diese protektiv.

After the addition of external microglia cells until 4 h after an insult, these cells act as neuroprotectives.
With 2-photon-konfocal microscopy we could show the migration of these cells into the slice and cell-cell contacts between microglia cells and neurons.

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