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  VEGF/VEGFR2 signaling regulates hippocampal axon branching during development.

Luck, R., Urban, S., Karakatsani, A., Harde, E., Sambandan, S., Nicholson, L., et al. (2019). VEGF/VEGFR2 signaling regulates hippocampal axon branching during development. eLife, 8: e49818. doi:10.7554/eLife.49818.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0005-70D3-E Version Permalink: http://hdl.handle.net/21.11116/0000-0005-70D6-B
Genre: Journal Article

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 Creators:
Luck, R., Author
Urban, S., Author
Karakatsani, A., Author
Harde, E., Author
Sambandan, S.1, Author              
Nicholson, L., Author
Haverkamp, S., Author
Mann, R., Author
Martin-Villalba, A., Author
Schuman, E. M., Author
Acker-Palmer, A., Author
de Almodovar, C. R., Author
Affiliations:
1Laboratory of Neurobiology, Max Planck Institute for Biophysical Chemistry, Max Planck Society, ou_3049887              

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 Abstract: Axon branching is crucial for proper formation of neuronal networks. Although originally identified as an angiogenic factor, VEGF also signals directly to neurons to regulate their development and function. Here we show that VEGF and its receptor VEGFR2 (also known as KDR or FLK1) are expressed in mouse hippocampal neurons during development, with VEGFR2 locally expressed in the CA3 region. Activation of VEGF/VEGFR2 signaling in isolated hippocampal neurons results in increased axon branching. Remarkably, inactivation of VEGFR2 also results in increased axon branching in vitro and in vivo. The increased CA3 axon branching is not productive as these axons are less mature and form less functional synapses with CA1 neurons. Mechanistically, while VEGF promotes the growth of formed branches without affecting filopodia formation, loss of VEGFR2 increases the number of filopodia and enhances the growth rate of new branches. Thus, a controlled VEGF/VEGFR2 signaling is required for proper CA3 hippocampal axon branching during mouse hippocampus development.

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Language(s): eng - English
 Dates: 2019-12-23
 Publication Status: Published online
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 Rev. Method: Peer
 Identifiers: DOI: 10.7554/eLife.49818
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Title: eLife
Source Genre: Journal
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Pages: 24 Volume / Issue: 8 Sequence Number: e49818 Start / End Page: - Identifier: -