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. 2017 Apr 28;7:1256. doi: 10.1038/s41598-017-01218-0

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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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Lovastatin does not rescue learning deficits or increased pERK level in HRas ^G12V/G12V mice. (A) Average latency to platform for each day of training, per genotype. A Significant effect of learning on the latencies of all groups was observed (within subject comparison: effect of time: F _1,58 = 46.80, P < 0.01). On average, HRas ^G12V/G12V mice (both groups: lovastatin and vehicle treated) showed significantly longer latencies compared to wild-type littermates (between subjects comparison: effect of genotype: F _1,58 = 5.89, P < 0.05). No effect of treatment on latencies was observed (between subjects comparison: effect of treatment: F _1,58 = 0.23, P = 0.63). (B) Probe trial data of watermaze learning shows that lovastatin did not rescue the learning deficit in HRas ^G12V/G12V mice (effect of treatment: P = 0.76; genotype*treatment interaction P = 0.79). TQ = target quadrant, RQ = adjacent right quadrant, LQ = adjacent left quadrant, OQ = opposite quadrant. Heat plots represent all search tracks combined, in which the color indicates the mean time spent at that position in the pool. Data are presented as mean ± SEM. *P < 0.05. NS: Not significant. Number of mice: vehicle group wild-type n = 17; HRas ^G12V/G12V n = 12; treated group: wild-type n = 17; HRas ^G12V/G12V n = 14. (C) Western blots of hippocampal lysates of the WT and HRas ^G12V/G12V mice showing an increased pERK level in untreated HRas ^G12V/G12V mice, but no effect of lovastatin on pERK level. (D) Quantification of Western blots. A significant effect of genotype was found in pERK level (F _1,20 = 6.48, P < 0.05). No main effect of treatment on pERK could be detected (F _1,20 = 0.21, P = 0.65; interaction genotype*treatment: F _1,20 = 0.08, P = 0.78). Data are presented as mean ± SEM normalized to vehicle group wild-type. n = 5; HRas ^G12V/G12V n = 5; treated group: wild-type n = 7; HRas ^G12V/G12V n = 7. Three mice per group are depicted in the example blot. Statistical test: two-way MANOVA.