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. 2017 Sep 20;7:11935. doi: 10.1038/s41598-017-12184-y

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© The Author(s) 2017

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 SNL induced hypofunction and WTD mediated remission of the glutamate system in the hippocampus CA3 region on D21. Tissues on the right side are analyzed (*P < 0.05, **P < 0.01, ***P < 0.001).(A)Alternated expression of glutamate and γ-GABA (Mean ± S.E.M, N = 5). (B) Altered expression of vGLuT1 (Mean ± S.E.M, 4–5 mice per group), using GAPDH as the loading control. (C) Altered expression of NR1, NR2A, NR2B, GluR1 and GluR2 (Mean ± S.E.M, 3 mice analyzed in Sham/WTD group and 6 in SNL), using GAPDH as the loading control. The gel pictures in 4B and C have been cropped and the original full-length gels are presented in supplementary Fig. S3. (D) The quantification of BDNF and GluR1/GluR2 co-localization CA3 pyramidal neurons by double immunofluorescence (Mean ± S.E.M, N = 3), scale bar 200 μm.