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. 2018 Jan 29;8:1829. doi: 10.1038/s41598-018-20271-x

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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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The α7-nAChR is upregulated on neurons, but not microglia, isolated from the striatum of gp120-tgm. Striatal neurons and microglia were isolated from WT and gp120-tgm adult mice’s brain. Cells were incubated with (A) CD90 (neuronal marker – green) or (B) CD80 (microglia marker - green), Bgtx Alexa 555 (α7-nAChR marker – red), and DAPI (nucleus marker – blue), to then measure fluorescence levels on a confocal microscope (40x). (A) Results demonstrate an increase in Bgtx binding, which is limited to neurons (n = 5 mice/strain), indicating an increase in α7-nAChR expression levels. Quantification of fluorescence shows a 3-fold increase in α7-nAChR expression on striatal neurons from gp120-tgm mice. (B) Microglia (n = 3 mice/strain) also express α7-nAChR but do not deviate significantly on fluorescence intensity. Results are shown as mean ± SEM values. Unpaired Student’s t-test, **P ≤ 0.01. Scale bar = 40 μm for all images in panels A and B.