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. 2022 Aug 31;100(10):1493–1508. doi: 10.1007/s00109-022-02250-y

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© The Author(s) 2022

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/.

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Fig. 7 — Mice with induced deletion of neutral sphingomyelinase 2 are resistant to stress-mediated inhibition of PLD and phosphatidic acid in the hippocampus. Mice induced to be deficient for neutral sphingomyelinase 2 (i.-Nsm 2^fl/fl) and not induced control littermates (n.i.-Nsm 2^fl/fl) were stressed with either glucocorticosterone (GC) or chronic unpredictable environmental stress (CUS) or were left untreated. Deletion of neutral sphingomyelinase 2 was induced by tamoxifen injection. PLD activity A and phosphatidic acid concentrations B in the hippocampus were determined. Displayed are the mean ± SD from each 8 animals. ***P < 0.001, ANOVA and post hoc Tukey test