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. 2018 Jul 30;9:2968. doi: 10.1038/s41467-018-04389-0

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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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Fig. 6 — Blocking EP-mediated oxidative stress and p38 activation rescued Aβ-induced synaptic loss. a, b Brain slices from 3-month-old non-Tg or Tg Sh3gl2 mice were perfused with Aβ (50 nM) for 2 h, and then subjected to immunoblotting analysis for synaptojanin (a) and synaptophysin (b) in the indicated groups of brain slices. β-Actin served as protein loading controls. The upper panel displays quantification of immunoreactive bands for the corresponding protein relative to β-actin. Data are expressed as fold change relative to the non-Tg vehicle control group. Data are shown as mean ± s.e.m., n = 3 per group (one-way ANOVA in a, b). c, d The Tg Sh3gl2 brain slices from 3-month-old mice were perfused with Aβ (50 nM) for 2 h with/without pretreatment of 500 nM EUK-134 (EUK), 1 μM SB203580 (SB), or 1 µM MitoTEMPO (TEMPO) for 5 min. Immunoblotting for synaptojanin (c) and synaptophysin (d) in the indicated groups of brain slices. The upper panel displays the quantification of immunoreactive bands for the corresponding protein relative to β-actin. Data are expressed as fold change relative to Tg Sh3gl2 vehicle control group. Data are shown as mean ± s.e.m., n = 3 per group (one-way ANOVA in c, d). Fourteen-day in vitro cultured cortical neurons, either non-Tg or Tg Sh3gl2, were treated with 50 nM Aβ for 24 h, with or without 500 nM EUK-134, 1 μM SB203580, or 1 μM MitoTEMPO pretreatment for 1 h before the addition of Aβ. The numbers of synaptophysin-positive clusters were significantly decreased in Aβ-treated Tg Sh3gl2 neurons compared to vehicle-treated non-Tg neurons in e–h. Treatment with EUK-134, or SB203580, or MitoTEMPO, inhibited Aβ-induced synaptic loss in cultured EP overexpression neurons (g, h). Representative images for synaptophysin (green), MAP2 (red), and nuclei (blue) in the indicated groups of neurons are shown in e, g. Scale bars, 50 μm. Quantifications of synaptophysin-positive clusters per 10 μm of dendrites are shown in f, h. Data are shown as mean ± s.e.m., n = 12 cells for each group (one-way ANOVA in f, h)