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. 2020 Jan 9;10:99. doi: 10.1038/s41598-019-57085-4

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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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Spontaneous endocytosis in not altered in Nampt^−/− cKO mice. (A–C) Motor endplate and nerve terminal from Nampt^f/f (A), Nampt^−/− cKO and NMN-treated Nampt^−/− cKO mice (B,C). nAChRs were labeled with α-BTX conjugated with Alexa 555 (top row) and nerve terminal of the corresponding motor endplate were stained with FM1-43 dye (middle row). Merged images of NMJ from α-BTX and FM1-43 images were shown in bottom row. Images were taken 30 minutes of incubation without nerve stimulation. (D) Mean fluorescence increase in nerve terminal of Nampt^f/f (29.6 ± 2.4, n = 34), Nampt^−/− cKO (30.0 ± 2.9, n = 27), and NMN-treated Nampt^−/− cKO (29.9 ± 2.9, n = 36) mice. n is the number of nerve terminals from 3–4 mice.