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. 2018 Mar 15;8:4641. doi: 10.1038/s41598-018-22848-y

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© The Author(s) 2018

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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KA induced excitotoxic injury kills RGCs in a dose independent manner. RGC loss was quantified 7 days after intravitreal injection of KA. (A,B) The RGC specific marker, TUJ1, was used to label RGCs in flat-mounted retinas 7 days after a 2 μl intravitreal injection of either PBS (vehicle control) or 10 mM, 12 mM, 15, or 20 mM of KA into C57BL/6 J mice (n = 14 for PBS control, n = 6 for 10 mM KA, n = 4 for 12 mM KA, n = 5 for 15 mM KA, n = 4 for 20 mM KA). Quantification of TUJ1 + RGCs showed that KA insult caused a dose independent loss of RGCs. All KA concentrations caused a significant decrease in RGC number (*p < 0.001 for all concentrations compared to control). Scale bar: 50 μm.