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. 2023 Jun 5;26(6):1032–1041. doi: 10.1038/s41593-023-01316-5

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© The Author(s) 2023

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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Extended Data Fig. 1 — a, b, LSD binds with high affinity to mouse (a) and human (b) TrkB. c, LSD displays a slow dissociation constant from TrkB WT, but fast dissociation kinetics from Y433F. d, Protein sequences of TrkA and TrkB TMDs of different species. e, BDNF induces a shift in fluorescence of GFP-tagged TrkB in MST. f, Ketamine and R,R-HNK displace LSD from TrkB at high concentrations, but not ketanserin or M100907. g, Psychedelics, but not ketanserin, displace R,R-HNK binding to TrkB with nM concentrations. h, Lisuride displaces LSD from its TrkB binding site, but other LSD-related compounds (cabergoline, dihydroergotamine) fail to do so. Negative control compounds chlorpromazine and diazepam also fail to displace LSD. i, MST confirms lisuride binding to TrkB. Data shown as mean ± s.e.m, *P < 0.05. Detailed statistics reported in Supplementary Table 1.