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. 2021 Jan 19;12:447. doi: 10.1038/s41467-020-20666-3

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© The Author(s) 2021

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. 7 — The schematics depict ChP NKCC1-mediated K⁺ and water clearance from CSF in neonatal mice, in comparison to the adult scenario. For simplicity and clarity, only K⁺ is depicted among all ions and only NKCC1 and Na⁺/K⁺-ATPase are included. Neonatal (P0-7, above) ChP has higher pNKCC1 expression than adult ChP, albeit lower total NKCC1. Neonatal CSF [K⁺] is 2–3 fold higher than adult. With similar [Na⁺] and [Cl⁻], this [K⁺] difference is sufficient to alter the total Nernst potential of epithelial cells and bias NKCC1 transport of K⁺, together with water, out of CSF and into the ChP in neonates.