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. 2020 May 6;11:29. doi: 10.1186/s13229-020-00340-7

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Chronic rapamycin treatment reversed the deficit in synaptic inhibition. a Diagram of experimental paradigm of chronic i.p. treatment of Nkx2.1^Cre/wt;Tsc1^f/wt mutant and Nkx2.1^Cre/wt control mice with 5 mg/kg rapamycin (or vehicle) and recording of synaptic inhibition of pyramidal cells by Nkx2.1 interneurons. b Representative western blots and summary graph showing reduced phosphorylation of ribosomal protein S6 (p-S6; relative to total S6) in hippocampal lysates obtained 24 h after 5-day treatment of control mice with rapamycin or vehicle (n = 3 separate experiments in each group; unpaired t test, ***p < 0.001). c, d Representative traces (c) and summary graph (d) of input-output function of IPSCs evoked in CA1 pyramidal cells in slices from Nkx2.1^Cre/wt;Tsc1^f/wt mutant (red) and Nkx2.1^Cre/wt control (black) mice that received vehicle (filled symbols) or rapamycin (open symbols). Chronic treatment with rapamycin reversed the reduction of IPSC amplitude in mutant relative to control mice (n = 9 cells in 4 animals for vehicle-treated and 7 cells in 3 animals for rapamycin-treated Wt mice (Nkx2.1^Cre/wt;Tsc1^wt/wt); n = 6 cells in 2 animals for vehicle-treated and 5 cells in 4 animals in rapamycin-treated Tg mice (Nkx2.1^Cre/wt;Tsc1^f/wt); 3-way ANOVA, Bonferroni tests, ***p < 0.001)