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. 2025 Jun 14;82(1):234. doi: 10.1007/s00018-025-05740-7

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© The Author(s) 2025

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 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/.

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Fig. 6 — CACNA1A loss-of-function caused by Y1854X mutation impairs neuronal network synchronization. (A, B) Raster plots (top) and array wide firing rate graph (bottom) showing 60 s of spontaneous activity recording at 28, 42 and 60 DIV in control (A) and Y1854X (B) neuronal cultures. The raster plot y-axis represents electrodes (from 0 to 4096), and each dot indicates a detected spike. The array wide firing rate quantifies the level of activity shown in the above raster plots and highlights the appearance of synchronous network events only in the control (green peaks at 42 and 60 DIV). (C) Graphs comparing the activity of control and mutated iPSC-derived neurons in terms of number of active electrodes, mean firing rate, mean bursting rate, mean burst duration, percentage of random spikes, percentage of bursting channels, network burst rate, and network burst duration. Data are shown as mean ± SEM. *, p < 0.05; **, p < 0.01 vs control (Student’s t test, n = 3–6 replicates for each time points and sample)