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. 2022 Feb 2;12:1820. doi: 10.1038/s41598-022-05937-x

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© The Author(s) 2022

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 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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Ketamine-induced changes in the dHPC phosphoproteome of proestrus and diestrus female rats. (A) Venn diagram depicting the number of phosphoproteins with significant estrous cycle-dependent differential abundance between ketamine (KET)- and saline (SAL)-treated proestrus or diestrus female rats. Red arrows indicate greater levels observed in KET- vs. SAL-treated rats. (B) Volcano plots showing significant KET-induced alterations in dHPC phosphoprotein abundance in proestrus (left) and diestrus (right) female rats. Log₂(Fold Change) values > 0 (red) indicate higher—and those < 0 (green) lower—abundance in KET-treated rats compared to SAL groups. Points above the horizontal dashed line represent proteins with p < 0.05 (FDR threshold set at 1%). (C) Heat map illustrating fold change of phosphoproteins significantly affected by KET in either proestrus or diestrus female rats. Top 10 most significant (p < 0.05) gene ontology (GO) enrichment terms per category of phosphoproteins with significant KET-induced differential abundance in proestrus (D) and diestrus (E) female rats. Heat map (C) was produced in GENE-E (Broad Institute; https://software.broadinstitute.org/GENE-E/).