(A) Representative extracellular DC potential shifts recorded simultaneously from cortex and striatum in female WT and homozygous R192Q and S218L mutant mice. SD was not observed to propagate into the striatum in any of the WT mice. A substantial proportion of CSDs propagated into the striatum in R192Q and to a greater extent in the S218L mutant. Calibration bars: vertical, 20 mV; horizontal, 10 minutes. (B) The frequency of SDs during continuous topical KCl application (300 mM) to the occipital cortex. CSD frequency (gray bars) was substantially higher in S218L and to a lesser extent in R192Q mutant mice than WT. They were higher in females compared with males and homozygous FHM1 mutants compared with heterozygotes (see Figure 1). CSDs readily propagated into striatum (black bars) in both FHM1 mutant strains, but never in the WT. Striatal propagation was more frequent in S218L (lower graphs) compared with R192Q mutants (upper graphs) and in females (right) compared with males (left), with an allele dosage relation (see Table 2 for latencies between cortical and striatal SDs). Covariance analysis revealed that 83% of the variance of striatal SD frequency was explained by the independent variables mutation, genotype, and sex (see Methods). n = 3–8 mice per group as shown within each bar. Data are mean ± standard deviation. *P < 0.01 versus male; ^†P < 0.001, ^§P < 0.05 versus heterozygous mutants; ^‡P < 0.01 versus R192Q males.