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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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Jnk2^−/−Jnk3^−/− nulls do not have attenuated RGC loss after excitotoxic injury. (A) Representative images showing TUJ1 immunolabeled cells in the GCL of Jnk2Jnk3 deficient mice 7 days after intravitreal NMDA or PBS injection, revealing significant RGC loss in both wildtype (Jnk2^+/?Jnk3^+/?) and Jnk2^−/−Jnk3^−/− deficient mice after NMDA insult (n = 4 for PBS WT, n = 4 for NMDA WT, n = 3 for PBS Jnk2^−/−Jnk3^−/−, n = 3 for NMDA Jnk2^−/−Jnk3^−/−). (B) Quantification of TUJ1 + RGCs confirmed that Jnk2^−/−Jnk3^−/− deficient mice had a similar loss of RGCs compared to wildtype mice 7d after NMDA injection (*p ≤ 0.001 for comparison between PBS and NMDA; p ≥ 0.9769 comparing WT to Jnk2^−/−Jnk3^−/− NMDA; ns between genotypes; two-way ANOVA, Tukey’s multiple comparisons test). Scale bar: 50 μm.