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. 2024 Sep 12;14:372. doi: 10.1038/s41398-024-03059-8

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 6 — A Power spectrum at electrode Pz averaged across all subjects during baseline (pre-drug) eyes-open, baseline eyes-closed, and eyes-closed at t = 2 h. after psilocybin administration. Note the prominent alpha peak (8–12 Hz) during pre-drug eyes-closed that is suppressed during pre-drug eyes-open and during eyes-closed with psilocybin. Data clouds represent standard errors of the mean. B Eyes-closed alpha power ratio (psilocybin/baseline) for each participant as a function of target midazolam (Midaz) dose. The two participants who exhibited memory impairment in Fig. 4 are indicated by filled symbols. C Distribution of alpha power across the EEG electrode array showing that eyes-closed alpha during baseline (center) is focused in the back of the brain and is profoundly suppressed at t = 2 h. after psilocybin administration.