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. 2017 May 22;7:2254. doi: 10.1038/s41598-017-02505-6

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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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TBI triggered an enduring increase in astrocytic A_2AR expression in the contralateral hippocampal CA1 region. Compared with the SHAM group (a), the expression of A_2ARs increased in both astrocytes and neurons in the contralateral hippocampal CA1 area 7 d (b) after TBI. (c) The up-regulation of A_2ARs was still obvious in astrocytes 4 weeks after TBI. Scale bar: 100 μm. (d) The expression of GFAP and A_2ARs at 1 d, 3 d, 7 d, and 4 weeks after TBI was analysed and quantified (e,f) using western blotting. n = 4 per group. Data represent mean ± s.e.m., ^*p < 0.05 compared with the SHAM group, ^nsp > 0.05 compared with the SHAM group, one-way ANOVA. Full length blots are presented in Supplementary Figure S1.