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. 2019 Feb 7;9:1633. doi: 10.1038/s41598-018-38208-9

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© The Author(s) 2019

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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Improved neuromuscular junction pathology in treated SMN∆7 mice. LDN-2014 (n = 4, 20 mg/kg) or vehicle (n = 4) were administered by IP daily until P7. Unaffected control mice (n = 4) were sacrificed at same age. (A) Representative immunohistochemistry of NMJs of the individual cohorts. Neurofilament and synaptic vesicle are shown in green. Acetylcholine receptors are stained with α-Bungarotoxin (red). (B) Quantification of endplate occupancy of n = 4 per group. (C) Percentage of NMJs that are fully occupied in vehicle and LDN-2014 treated groups compared to the untreated cohorts. Data was analyzed using by one-way ANOVA and statistical significance is represented by “*”p ≤ 0.05; “**”p ≤ 0.01; “***”p ≤ 0.001; “****”p ≤ 0.001; ^“ns”p > 0.05 and expressed as S.E.M.