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. 2021 May 12;12:2764. doi: 10.1038/s41467-021-22850-5

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© The Author(s) 2021

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. 3 — a Directionality consistency values (DC; dots) across trials for the 1.9 Hz peak frequency in Participant 5 (n = 43 trials) with timepoints locked to the visual stimulus at time zero, colored as average direction of travel (circular mean, saturation proportional to maximum DC, direction according to color wheel: I: inferior, P: posterior, S: superior, A: anterior) over the hippocampal surface (pixels in lane at top: FDR-corrected Rayleigh test p-value, p_FDR; see scale bar). The propagation strength across trials was estimated by mean R² (gray superimposed line: separate y-axis at right) which was roughly similar when trials were aligned in direction or not (high or low DC). Directional distributions are shown below for two example timepoints (dotted lines). Roughly 700 ms after the stimulus waves abruptly begin to align antero-inferiorly across trials (strongest p_FDR = 3.2⁻⁵, Rayleigh). b DC now locked to speech onset (time zero). Alignment of propagation across trials similar to (a) is evident again shortly before speech (strongest p_FDR = 0.0243, Rayleigh) and resolves back to baseline levels after speech onset. c Trials in (a and b) were grouped by reaction time (fast or slow, median split). Fast reaction time trials increased in DC significantly after the stimulus (strongest p_FDR = 0.0049, Rayleigh; see scale bars) and (d) around speech onset (strongest p_FDR = 5.6⁻⁶, Rayleigh), whereas slow reaction time trials did not (empty p_FDR lanes). e Trial rasters of analytic amplitude for the 1.9 Hz frequency described in (a), averaged across trials in bottom panel (mean: black trace; blue envelope: standard deviation) with a subtle increase peaking at ~600 ms, returning to baseline as DC in (a) begins to increase. f Similar to (e) now locked to speech onset (time zero) with amplitude staying roughly at baseline during DC changes in (b) (mean: black trace; blue envelope: standard deviation). g, h Illustrate the 13.8 Hz peak frequency (similar to (a) and (b)) in the same participant with limited DC value trends (strongest p_FDR = 0.0119, Rayleigh) that dissipate by ~500 ms into trials.