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. 2020 Jul 29;17:226. doi: 10.1186/s12974-020-01894-2

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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. 2 — IFNAR1 deficiency partially ameliorates the loss of presynaptic terminals preferentially in the hippocampus of females. Representative images of the cortex (a; layer 3) and hippocampus (b; CA1) immunolabeled for neuronal synaptophysin (SYP); deconvolution microscopy; scale bar, 40 μm. c, d Quantification of microscopy data obtained in the cortex and hippocampus of sagittal brain sections of 12–14-month-old mice. Genotypes: WT (WT), HIVgp120tg (GP), IFNAR1KO (KO), and IFNAR1KO × gp120 (KOGP). Values are presented in combined box-dot plots with the 25th and 75th percentiles. The middle line of the box shows the median, and the mean is indicated by a “+”; ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05; ANOVA and Tukey’s HSD post hoc test; n = 6 animals (3 males and 3 females) per group/genotype (total n = 24 animals)