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. 2020 Apr 24;10:6956. doi: 10.1038/s41598-020-63255-6

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© The Author(s) 2020

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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NLGN1 absence induces neuronal loss after Aβo_1-42 exposure. (A) Representative IF images of NeuN staining (green) in the full hippocampus. The approximate location of the counting area is indicated by the yellow rectangle. Magnification 2.5X. (B) Representative IF images of NeuN staining (green) in the DG, where neuron counting was conducted. One image per group is showing approximately the same position within the DG. Magnification 40X. (C) Quantification of the area covered by the counting zone, which did not significantly differ between groups (two-way ANOVA Genotype main effect: F_1,20 = 0.6, p = 0.4; Treatment main effect: F_1,20 = 0.1 p = 0.8; Genotype-by-Treatment interaction: F_1,20 = 0.2, p = 0.7). (D) Number of NeuN-marked cells counted in the DG target area showed a significant Genotype-by-Treatment interaction (two-way ANOVA F_1,20 = 8.1, p = 0.01), with the KO Aβ group showing a significant difference in the number of immunoreactive cells in comparison to all other groups (star indicates planned comparisons). The number of mice is 6 per group.