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. 2018 Aug 13;8:12003. doi: 10.1038/s41598-018-30524-4

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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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Inhibition of ERK1/2 phosphorylation rescued the restraint stress-induced working memory impairment. A brain penetrant ERK1/2 inhibitor, SL327, was injected i.p. 30 min before restraint stress followed by brain preparation (a,b) or Y maze test (c,d). (b) Western blot representative images and the graphical representation of pERK1/2 divided by ERK1/2 bands intensity after SL327 treatment and restraint stress (n = 5). Quantifications of pERK1/2/ERK1/2 were presented as the fold change normalized by control. (d) Y-maze test showing the spontaneous alterations of each group (n = 12). All data are expressed as the mean ± S.E.M using bar graphs. All statistical analyses were performed using two-way ANOVA test and Bonferroni’s multiple comparison post hoc analysis. * is p < 0.05, ** is p < 0.01, *** is p < 0.001. Con: vehicle control group, RS: restraint stress group.