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. 2020 Dec 10;15:72. doi: 10.1186/s13024-020-00419-y

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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 — Dramatic increases of apoptotic interneurons in the cerebral cortex of IN-PS cDKO mice. a-d Immunohistochemical analysis shows co-localization of active caspase-3- and GAD67-immunoreactivity (yellow arrowheads) in the neocortex and hippocampus of IN-PS cDKO mice. The few apoptotic cells (active caspas-3+) present in the neocortex and hippocampus of the control brain tend to be GAD67- (white arrowheads). Inserts show higher power views of the boxed areas. e Quantification of apoptotic interneurons (active caspase-3+/GAD67+) and apoptotic non- interneurons (active caspase-3+/GAD67-) in the neocortex and hippocampus of control and IN-PS cDKO mice at the age of 9 months. IN-PS cDKO mice show dramatic increases of apoptotic interneurons (active caspase-3+/GAD67+) in the neocortex (p < 0.0001, Student’s t-test) and hippocampus (p = 0.0002), compared to controls. There is no significant difference in the number of apoptotic non-interneurons (active caspase-3+/GAD67-) in the neocortex (p = 0.47, Student’s t-test) and hippocampus (p = 0.11) between IN-PS cDKO and control mice. f-i The few cells immunoreactive for both active caspase-3 and CaMKIIα are shown (cyan arrowheads) in the neocortex and hippocampus of control and IN-PS cDKO brains, whereas most apoptotic cells are non-excitatory neurons (active caspase-3+/CaMKIIα-) present in IN-PS cDKO brains (white arrowheads). Inserts show higher power views of the boxed areas. j Quantification of apoptotic excitatory neurons (active caspase-3+/CaMKIIα+) and apoptotic non-excitatory neurons (active caspase-3+/CaMKIIα-) in the neocortex and hippocampus of control and IN-PS cDKO mice at the age of 9 months. While there are dramatic increases of apoptotic non-excitatory neurons in the neocortex (p < 0.0001, Student’s t-test) and hippocampus (p < 0.0001) of IN-PS cDKO mice, compared to controls, there is no significant difference in the number of apoptotic excitatory neurons in the neocortex (p = 0.36, Student’s t-test) and hippocampus (p = 0.45) of IN-PS cDKO mice, compared to controls. Scale bar: 100 μm. All data represent mean ± SEM. ns = no significance, ***p < 0.001, ****p < 0.0001