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. 2017 Nov 21;8:1668. doi: 10.1038/s41467-017-01709-8

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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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Fig. 5 — TrkB is required in adult NPCs to mediate the antidepressant effects of ketamine. a The quantification on BDNF immunoblots of dissected adult CA1 and DG regions shows the BDNF protein level significantly increases 1 h after saline (S) or ketamine (K) treatment. (n = 3; ***p < 0.0001 for CA1, ***p < 0.0001 for DG). b Nestin-creER^T2; TrkB flox/flox (TrkB^Nes) mice were induced with tamoxifen (TAM) three weeks before saline (Sal) or ketamine (Ket) treatment. BrdU pulses were administrated sixteen days before treatment, and mice were given behavior tests (BT) 1 h, 24 h or 1 week after treatment. c The percentage of newborn NeuN+/DCX− neurons in BrdU+ cells (two-way ANOVA, Tukey post hoc, ***p = 0.0001 for saline vs ketamine in control mice; **p = 0.0031 for ketamine-treated control vs TrkB^Nes; p = 0.2510 for saline vs ketamine in TrkB^Nes). d Percentage of newborn DCX+ cells (two-way ANOVA, Tukey post hoc, **p = 0.0048 for saline vs ketamine in control; *p = 0.0219 for ketamine treatment in control vs TrkB^Nes). e In the FST, TrkB^Nes mice respond to ketamine 1 h after treatment (two-way ANOVA, Tukey post hoc, **p = 0.0013 for saline vs ketamine in control mice and ***p < 0.001 for saline vs ketamine in TrkB^Nes). However, they do not retain the behavioral response at both (f) 24 h (two-way ANOVA, Tukey post hoc, ***p < 0.001 for saline vs ketamine in control mice and for ketamine treatment in control vs TrkB^Nes) and (g) 1 week (two-way ANOVA with unweighted mean analysis, Tukey post hoc, ***p = 1.773E-8 for saline vs ketamine in control mice and ***p = 2.633E−6 for ketamine treatment in control vs TrkB^Nes). (h) In the NSFT, the TrkB^Nes mice have a longer latency to feed compared with ketamine-treated control mice (two-way ANOVA, Tukey post hoc, ***p < 0.001 for saline vs ketamine in control mice (p = 0.0007) and for ketamine treatment in control vs TrkB^Nes (p = 0.0006)). i Cumulative feeding latency is measured (Mantel–Cox log-rank test ***p < 0.0001 for ketamine treatment in control mice compared with other groups). Dash-line highlights the time-point when all ketamine-treated control mice had eaten, compared with a significant lower percentage of mice in the other groups. j We observed no confounding effects on appetite (two-way ANOVA). Circles in solid color denote female mouse data points