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. 2022 Sep 29;23(1):125. doi: 10.1186/s10194-022-01495-9

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — FHM1 mutations altered visual evoked potentials, decreased multi-unit activity but preserved information visual processing. A (left) Representative scheme of the experimental design. Square-wave 1 Hz alternating gratings at different contrast levels (K) were used for visual stimulation. A linear 16-channels probe (with 50 μm spacing between electrodes) was inserted into mice (n = 12 for WT; n = 12 for FHM1) V1. (right) Mean CSDs across animals aligned by the earliest current sink. B Mean VEPs across contrast levels K for WT (orange) and FHM1 (green) mice, and their difference (black). Solid horizontal lines indicate intervals of significant difference (permutation cluster-based test). Shaded regions indicate SEM. C (top) Schematic representation of the features extracted from the VEPs. (bottom) clockwise from top left to bottom right: amplitude of N1 [mV] (2WA: group F = 0.83; K F = 19.62; interaction F = 0.46); magnitude of the downslope of the first negative deflection of the VEPs [mV/s] (2WA: group F = 13.03; K F = 4.16; interaction F = 2.32); latency of N1 [ms] (2WA: group F = 175.78; K F = 28.56; interaction F = 4.63); amplitude difference between P2 and N1 [mV] (2WA: group F = 52.68; K F = 17.47; interaction F = 1.08). * p < 0.05 Dunn-Sidak post hoc test. D Normalized MUA of WT (left) and FHM1 (middle) mice and their difference (right) across contrast levels (in the legend). E Peak amplitude of normalized MUA of WT (orange) and FHM1 (green). 2WA K: F = 16.56; group: F = 12.98; interaction: F = 2.55. *** p < 0.001 Dunn-Sidak post hoc test. F Mutual information about contrast levels carried across time by the MUA of WT (left, orange) and FHM1 (right, green). Gray lines indicate non-significant (indicated as n.s. in the colorbar legend) MI (p > 0.05 bootstrap test)