(A) Representative electrophysiological recordings showing increased frequency of slow (DC) potential shifts during repetitive CSDs in male and female homozygous R192Q or S218L mutants compared with WT mice evoked by topical KCl application (300 mM) for 30 minutes. The number of CSDs was substantially higher in FHM1 mutant strains compared with WT controls and in female mutants versus males. Calibration bars: vertical, 20 mV; horizontal, 10 minutes. (B) The impact of R192Q and S218L mutations, allele dosage, and sex on CSD frequency and propagation speed (upper and lower graphs, respectively). Higher CSD frequencies and propagation speeds were found in both FHM1 mutants, with values higher in S218L than in R192Q mutants and an allele dosage relation. CSD frequency was greater and propagation faster in females compared with males in both FHM1 mutant strains. No sex difference was found in WT mice. Covariance analysis revealed that 82% of variation in CSD frequency and 93% of variation in CSD propagation speed were explained by the independent variables mutation, genotype, and sex (see Methods). Numbers of mice per group are shown within the bars. HET, heterozygous; HOM, homozygous. Data are mean ± standard deviation. **P < 0.001, *P < 0.01 versus male in CSD frequency and propagation speed; ^†P < 0.001 versus WT and homozygous mutant; ^‡P < 0.001 versus WT and heterozygous mutant; ^§P < 0.001 versus corresponding R192Q genotype.