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. 2019 Jul 11;10(7):535. doi: 10.1038/s41419-019-1766-z

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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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Fig. 3 — a Coimmunostaining of Kidins220 and the Golgi apparatus marker GM130 in neurons treated with NMDA for the indicated times in the absence or presence of the NMDAR antagonist DL-AP5 (200 μM, 60 min). Nuclei were stained with DAPI. Merge confocal microscopy images and magnifications corresponding to the boxed areas are depicted. Scale bar: 10 μm. b, c Percentage of cells displaying colocalization of Kidins220 and GM130 and mean Pearson correlation coefficient (PCC) values, respectively, after 60 min of NMDA treatment, calculated in single optical sections obtained from the different conditions. d Merged magnified images of Kidins220 and GM130 coimmunofluorescence in neurons preincubated with cycloheximide (CHX; 200 μM, 240 min) before NMDA stimulation for 60 min. e, f Percentage of cells displaying colocalization of Kidins220 and GM130 and mean PCC values were calculated as above. Data shown are the means ± s.e.m of three independent experiments after counting n = 20–40 neurons. **p < 0.01, ***p < 0.001, Student’s t-test