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. 2020 Sep 14;26(7):3292–3301. doi: 10.1038/s41380-020-00878-1

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© The Author(s) 2020

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. 1 — Ketamine differentially altered functional connectivity between the groups, as reflected in VS-left dlPFC (a), DC-right vlPFC (b), DCP-pgACC (c), and VRP-left/right OFC (d) coupling. This was identified using group-by-treatment F–tests at a family-wise error (FWE) cluster-corrected threshold level of p < 0.05. Boxplots with individual data points and distributions [75] show that functional connectivity was increased in individuals with treatment-resistant depresssion (TRD) but reduced in healthy volunteers (HVs) post-ketamine relative to placebo (a–d). Resting-state functional magnetic resonance imagining scans (rsfMRI) were acquired 2 days after each infusion. VS ventral striatum; DC dorsal caudate; DCP dorsal caudal putamen; VRP ventral rostral putamen; dlPFC dorsolateral prefrontal cortex; vlPFC ventrolateral prefrontal cortex; pgACC perigenual anterior cingulate cortex; OFC orbitofrontal cortex; L left; R right; FWE family–wise error.