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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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AVP V1a and V2 receptor antagonist reverts the EAE-induced blood-brain barrier hyper-permeability to Evans blue. Graphs show the concentration (µg/g of tissue) of Evans blue dye in the brain (a) and spinal cord (b) of Intact Control (IC). Experimental Autoimmune Encephalomyelitis (EAE) and EAE plus conivaptan at 3 mg/kg (CO) (n = 6 per group). (a) Conivaptan treatment significantly reduced Evans blue dye concentration in the brain as compared with the EAE group. (b) Graph shows a trend toward a decrease in Evans blue extravasation in animals treated with conivaptan, but no significant differences were found as compared with the EAE group. (c) Representative images of Evans blue extravasation in the brain and spinal cord of intact control (IC), Experimental Autoimmune Encephalomyelitis (EAE) and EAE plus conivaptan at 3 mg/kg (CO) groups. Mean ± SD, Kruskal-Wallis test and Dunn´s post hoc test, **p < 0.01.