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. 2019 Mar 12;9:4245. doi: 10.1038/s41598-018-37819-6

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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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Effects on IAN regeneration with a local administration of anti-Sema3A antibody. (a,b) Nerve regeneration demonstrated with PGP9.5 immunohistochemistry at postoperative (PO) 3 days. (a) Nerve fibers extending in random direction from the lesion are observed in a vehicle control treated with physiological saline (PS). In contrast, administration of anti-Sema3A antibody eliminates the radial extension of injured axons, resulting in axonal regeneration (b). (c) A comparison of DiI-labeled neurons in the trigeminal ganglion with a local administration of PS and Sema3A antibody to the transected site of IAN. The graph (d) shows that the number of DiI-labeled neurons is greater in anti-Sema3A antibody-treated animals than in vehicle control animals with a significant difference (Student’s t-test, *p < 0.05). Scale bars = 100 µm (a–c).