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. 2020 Jan 16;10:467. doi: 10.1038/s41598-019-57134-y

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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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Conivaptan treatment reverts the EAE-induced blood-brain barrier hyper-permeability to 10-kDa FITC-dextran. Graphs show the concentration (mg/g of tissue) of 10-kDa FITC-dextran in the cortex (a), hippocampus (b), basal nuclei (c), vermis (d), and spinal cord (e) of intact control (IC), Experimental Autoinmmune Encephalomyelitis (EAE) and EAE plus conivaptan at 3 mg/kg (CO) (n = 6 per group). Mean ± SD. One-way ANOVA test and Tukey´s post hoc test, *p < 0.05 and **p < 0.01.