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. 2020 Mar 9;11:1313. doi: 10.1038/s41467-020-15041-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Panels illustrate the suggested cellular mechanisms and effects of EPO/EPOR in CA1 (hypotheses and respective figure created by Hannelore Ehrenreich). a Functional challenge of pyramidal neurons (blue) via, e.g., learning of new complex tasks provokes physiological hypoxia of the involved neurons. Hypoxia in turn induces neuronal production/release of EPO, which initiates differentiation of diverse non-proliferating precursors (red) with currently unknown identity to neurons. b Neuronal EPO binds in an auto/paracrine manner to EPOR on pyramidal neurons (blue), leading to an increase in dendritic spines. EPO simultaneously binds to EPOR on likely diverse neighboring cells (red), ready to differentiate into neurons on demand. Together, these integrative steps may explain the consistently found improvement of cognitive function under rhEPO treatment and, even more importantly, delineate physiological mechanisms, accomplishing lasting adaptation to challenge via the brain EPO system.