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. 2017 Jun 22;7:4040. doi: 10.1038/s41598-017-04355-8

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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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Effect of contextual fear memory retrieval on CaMK2N1 and CaMK2N2 dorsal hippocampi mRNA levels. (a) Animals (n = 10) were conditioned with 3 foot shocks (0.7 mA, 2 s). Half of the conditioned animals retrieved contextual fear LTM for 5 minutes 24 hours after conditioning (TR + TE). All animals were sacrificed 24.5 h after conditioning and mRNA expression in dorsal hippocampi was studied using RT-qPCR analysis. Retrieval of contextual fear LTM significantly upregulated CaMK2N1 expression. (b) CaMK2N2 mRNA levels were not altered by reactivation of contextual fear LTM. (c) A different cohort of animals (n = 12) was conditioned with 5 foot shocks (0.7 mA, 2 s) and, as in panel (a), half of the animals retrieved contextual fear LTM. CaMK2N1 expression did not change by retireval of this stronger contextual fear LTM. (d) However, CaMK2N2 mRNA levels were significantly increased by LTM retrieval. Hence, the intensity of the unconditioned stimulus influences the effect that memory retrieval has on the expression of the two endogenous CaMKII inhibitors. Mean and S.E.M.; *P < 0.05; **P < 0.01.