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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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Deficiency of JUN does not protect RGCs after excitotoxic injury. To determine if JUN is required for NMDA induced RGC death, NMDA was injected into the vitreous of Jun deficient (Jun^fl/fl; Six3-cre⁺) mice. The number of surviving RGCs (TUJ1+ cells) were counted 7 days after intravitreal NMDA injection. (A) Representative images from flat mounted retinas stained with anti-TUJ1 show significant RGC loss in both wildtype (Jun^+/?; Six3-cre⁻) and Jun^fl/fl; Six3-cre⁺ mice after NMDA insult (n = 5 for PBS WT, n = 5 for NMDA WT, n = 6 for PBS Jun^fl/fl; Six3-cre⁺, n = 5 for NMDA Jun^fl/fl; Six3-cre⁺). (B) Quantification of TUJ1+ RGCs confirmed that Jun deficient mice had a similar loss of RGCs compared to wildtype mice 7d after NMDA injection (*p < 0.001, comparing 20 mM NMDA to PBS control; p = 0.9846 comparing WT to Jun^fl/fl; Six3-cre NMDA; ns between genotypes). Scale bar: 50 μm.