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. 2017 Sep 29;7:12412. doi: 10.1038/s41598-017-12603-0

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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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IPA analysis of the thalamic synaptic proteome. (A) Table of top 5 “diseases and disorders” and “molecular and cellular functions”. (B and C) Canonical pathways bar chart of representative pathways showing, (B) The percentage of upregulated and downregulated proteins within each pathway. Numbers on the top indicate the total number of proteins within the canonical pathway. (C) Significance of the association between the dataset and the canonical pathway (−log(p-value) and ratio) and z-score prediction of activation/inhibition (see Methods). Pathways highlighted in green and blue are associated to ROCK2 and HIBCH, respectively. (D) HIBCH and ROCK2 protein expression ratio across cortex (“less affected’) and thalamic (“degenerating”) synapses in these moderately affected Cln3 ^−/− mice (Cln3 ^−/−/WT). (E) HIBCH and ROCK2 protein expression is conserved in models of injury, following similar pattern of expression 24 hours post-injury when synapses start to degenerate².