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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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Overexpression of CaMK2N2 in dorsal hippocampi impairs memory formation but does not impair contextual fear LTM maintenance. (a) Dorsal hippocampi of mice were transfected with rAAV expressing either ZsGreen (n = 13) or CaMK2N2 (n = 11) under control of a synapsin 1 promoter. Contextual fear LTM was determined one day and 4 days after conditioning. No significant difference was observed. (b) Mice studied in (a) overexpressed CaMK2N2 mRNA in dorsal hippocampus (Control rAAV, n = 11; CaMK2N2 rAAV, n = 10). (c) Overexpression of CaMK2N2 mRNA did not alter CaMK2N1 mRNA levels (Control rAAV, n = 9; CaMK2N2 rAAV, n = 9). (d) Another cohort of animals was subjected to the same experimental design as in (a) with the exception that these animals were treated with a 60x more concentrated version of the CaMK2N2 rAAV solution (1.07 × 10¹³ GC/ml). In these mice CaMK2N2 overexpression reduced freezing scores in the first memory test, indicating impaired memory formation (Control rAAV, n = 11; CaMK2N2 rAAV, n = 10). (e) RT-qPCR analysis confirms effective overexpression of CaMK2N2 in dorsal hippocampi of CaMK2N2 rAAV 60x animals (n = 10) compared to Control rAAV (n = 11). (f) CaMK2N2 rAAV 60x treatment did not affect CaMK2N1 mRNA levels (Control rAAV, n = 11; CaMK2N2 rAAV, n = 10). (g) A final cohort of animals was first conditioned in the CFC paradigm and 24 hours later treated with the 60x CaMK2N2 rAAV solution. A period of 2 weeks was waited to allow the genetic information from the vector to be expressed, after which the fear memory of the context was tested twice. The two tests were apart from each other by 3 days, therefore they were executed 15 days and 18 days after CFC conditioning. No significant effect of 60x CaMK2N2 rAAV treatment was observed in the freezing behavior (Control rAAV, n = 8; CaMK2N2 rAAV, n = 7). (h) CaMK2N2 mRNA levels were increased after 60x CaMK2N2 rAAV treatment (Control rAAV, n = 8; CaMK2N2 rAAV, n = 7). (i) CaMK2N2 overexpression did not affect CaMK2N1 mRNA levels (Control rAAV, n = 8; CaMK2N2 rAAV, n = 7). Mean and S.E.M.; *P < 0.05; **P < 0.01; ***P < 0.001.