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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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Dlk deficiency does not protect RGCs from NMDA-induced death. (A) Representative images showing TUJ1 immunolabeled cells in the GCL of control (Dlk^+/+; Six3-cre⁻ or Dlk^+/fl; Six3-cre⁻) Dlk deficient (Dlk^fl/fl; Six3-cre⁺) mice 7 days after intravitreal NMDA or PBS injection (n = 4 for PBS WT; n = 3 for NMDA WT, n = 5 for PBS Dlk^fl/fl; Six3-cre⁺, n = 4 for NMDA Dlk^fl/fl; Six3-cre⁺). There was significant RGC loss in both control and Dlk deficient mice after NMDA insult. (B) Quantification of TUJ1 + RGCs showed that Dlk deficient mice had a similar loss of RGCs compared to wildtype mice 7d after NMDA injection (*p < 0.001 for comparison of PBS to NMDA; p ≥ 0.1843 for comparison between genotypes, ns between genotypes). Scale bar: 50 μm.