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MicroSynCom SIGNED

Mechanisms of Microglia Synapse Communication

Total Cost €

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EC-Contrib. €

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Project "MicroSynCom" data sheet

The following table provides information about the project.

Coordinator
DEUTSCHES ZENTRUM FUR NEURODEGENERATIVE ERKRANKUNGEN EV 

Organization address
address: SIGMUND FREUD STRASSE 27
city: BONN
postcode: 53127
website: www.dzne.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Total cost 1˙687˙476 €
 EC max contribution 1˙687˙476 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-09-01   to  2025-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    DEUTSCHES ZENTRUM FUR NEURODEGENERATIVE ERKRANKUNGEN EV DE (BONN) coordinator 1˙687˙476.00

Map

 Project objective

Microglia are the resident tissue macrophages of the brain and represent cells of the innate immune system. Looking at microglia from the immunological perspective, much is known about their role during inflammatory processes, factors that activate them and how they response e.g by releasing cytokines to mount an inflammatory response. This response has been shown to be detrimental during disease processes and lead to pruning/loss of synapses, a task microglia carry out also during development. Although microglia obviously play an important role in synaptic pruning and loss, it remains an open question, whether microglia are involved in the process of synapse formation under physiologic conditions. Therefore, the main hypothesis of MicroSynCom is that microglia represent the mediator of synapse formation or linker between pre- and post-synapse: sensing neurotransmitter release at highly active pre-synaptic sites and actively orchestrating the formation of new spines from the dendrite. I propose to investigate and reveal the underlying mechanisms of this tripartite microglia synapse communication process. Therefore, we will use two-photon stimulated emission depletion microscopy (2P-STED), novel viral and genetically encoded sensors for neurotransmitters, as well as optogenetic and chemogenetic manipulation tools. These methods will be combined with behavior test in freely moving, but also head-fixed mice to visualize microglia mediated synapse formation in awake mice. This will allow us for the first time to visualize, investigate and reveal the mechanisms establishing this novel role of microglia as the mediator of synapse formation in life animals and relate it to physiologically relevant neuronal network rewiring.

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The information about "MICROSYNCOM" are provided by the European Opendata Portal: CORDIS opendata.

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