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  Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin

Wakhloo, D., Scharkowski, F., Curto, Y., Butt, U. J., Bansal, V., Steixner-Kumar, A. A., et al. (2020). Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin. Nature Communications, 11: 1313. doi:10.1038/s41467-020-15041-1.

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 Creators:
Wakhloo, D.1, Author              
Scharkowski, F.1, Author              
Curto, Y.1, Author              
Butt, U. J.1, Author              
Bansal, V.1, Author              
Steixner-Kumar, A. A.1, Author              
Wüstefeld, L.1, Author              
Rajput, A., Author
Arinrad, S.1, Author              
Zillmann, M. R.1, Author              
Seelbach, A.1, Author              
Hassouna, I.1, Author              
Schneider, K.1, Author              
Qadir Ibrahim, A., Author
Werner, Hauke B., Author
Werner, H. B.2, Author              
Martens, H., Author
Miskowiak, K., Author
Wojcik, Sonja M., Author
Wojcik, S. M.3, Author              
Bonn, S., AuthorNacher, J., AuthorNave, Klaus Armin2, Author              Ehrenreich, H.1, Author               more..
Affiliations:
1Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173651              
2Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173664              
3Molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173659              

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Free keywords: Cellular neuroscience; Cognitive neuroscience
 Abstract: Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks—challenged by cognitive tasks—drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.

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Language(s): eng - English
 Dates: 2020-03-09
 Publication Status: Published online
 Pages: -
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 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41467-020-15041-1
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Title: Nature Communications
Source Genre: Journal
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Pages: 12 Volume / Issue: 11 Sequence Number: 1313 Start / End Page: - Identifier: ISSN: 2041-1723