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. Author manuscript; available in PMC: 2025 Jul 15.
Published in final edited form as: Genet Med. 2025 Jun 23;27(9):101506. doi: 10.1016/j.gim.2025.101506

Figure 5. Studying ELFN1 deficiency in animal models.

Figure 5.

A) Time-course of locomotor activity of wildtype, Elfn1+/−, knockout Elfn1−/− and heterozygous Elfn+/− mice in the open field. B) Quantification of the total locomotor activity in the open filed over 2 hours. C) Behavioral and (D,E,F) electrophysiological seizure analysis of MO-injected zebrafish larvae at 5 dpf. C) Behavioral data is compared to control MO (elfn1a+/+/elfn1b+/+) and expressed as cumulative duration in highly active state (mean ± SEM) (n control MO = 73, n elfn1a/elfn1b MO = 29-30). D,E,F) Electrophysiological epileptiform activity is assessed via non-invasive local field potential recordings (n control MO = 18, n elfn1a/elfn1b MO = 15-16). D) Data is visually analysed and expressed as the number of epileptiform events (mean ± SEM) and compared to control MO. E,F) Data is normalized against control MO and expressed as (E) normalized power spectral density (PSD) (mean ±SEM) per larva per 10 Hz frequency band from 1-150 Hz and as (F) normalized PSD (mean ±SEM) per larva within the 10-90 Hz region. Statistical analysis was performed using (C,D,E,F) non-parametric Kruskal-Wallis test with Dunn’s multiple comparisons test. Outliers were removed via the ROUT test (Q = 1%). Significance levels: * p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001.