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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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CXCR4 mediates the effects of gp120 on striatal neurons. Striatal neurons isolated from WT mice were treated with: 1) gp120_IIIB, 2) gp120_IIIB + AMD3100, or 3) gp120_IIIB + PD98059 for 48 hrs. Then, cells were incubated with Alexa Fluor 555 α-bungarotoxin to measure α7-nAChR expression levels by confocal imaging (20x). Treatment with gp120_IIIB induced an α7-nAChR upregulation on striatal neurons, which is abolished by pretreatment with a CXCR4 antagonist (AMD3100), suggesting that this upregulation is CXCR4-dependent. Additionally, blocking the Ras-Raf-MEK pathway (downstream signaling pathway of CXCR4) also abolished the gp120-induced α7-nAChR upregulation. n = 4 mice/treatment. Results are shown as mean ± SEM values. Matched One-Way ANOVA with Holm-Sidak’s post-test, *P ≤ 0.05.