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. 2019 Jan 22;2:32. doi: 10.1038/s42003-018-0277-2

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© The Author(s) 2019

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. 4 — Time-dependent changes in the hiM- and hiI-indexes in animals subjected to various putative risk events for neuropsychiatric disorders and in genetic mouse models of schizophrenia, bipolar disorder, ALS, and Alzheimer’s disease. a Pattern of changes in the hiM- and hiI-indexes in the mouse and rat hippocampus after treatment with kainite (seizure #1 (GSE1831) and seizure #2 (GSE4236)), in mouse cortex and astrocytes after middle cerebral artery occlusion (MCAO; ischemia #1 (GSE32529), ischemia #2 (GSE35338)), and in mouse cortex after CpG infection (GSE32529). b Pattern of changes in the hiM- and hiI-indexes of the spinal cord of an ALS mouse model with the SOD1(G93A) mutation. c Pattern of changes in the hiM- and hiI-indexes of the hippocampus and cortex of an Alzheimer’s disease mouse model with mutations in APP and PSEN1. d hiM- and hiI-indexes in mouse models of schizophrenia and bipolar disorder