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. 2020 May 12;9:18. doi: 10.1186/s40035-020-00194-2

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — The GluN2A restoration in APP/PS1 after Paroxetine treatment according to NMDAR-mediated synaptic current. a Representative traces of NMDAR EPSC recorded at +40mv (black) and in the presence of ifenprodil (red) or NVP-AAM007 (blue). b Effect of ifenprodil application on NMDAR EPSC amplitude and decay time constant. c Effect of NVP application on NMDAR EPSC amplitude and decay time constant. Scale bar: 250pA (vertical) × 100 ms (horizontal). n = 12–20 neurons from 3 to 5 mice for per group. The data of decay time is normalized to the NMDA. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; *** P < 0.001; two-way ANOVA with Sidak’s multiple comparison post hoc test