PMC

Numerical simulations show depolarization of mixed states consisting of coherently detected scatter signals. a, Depolarization increases with increasing diattenuation, μ, and yields a dependency on the input states. Δ_Q, Δ_U, Δ_V represent depolarization for horizontal, 45-deg and circular input polarization, respectively, while depolarization power (D) corresponds to the average of principle depolarization factors. The inset shows depolarization for a continuum of probing states on the Poincaré sphere for μ = 0.85. Colour bar represents depolarization, 0 – 1. b, Simulated depolarization for mixtures of depolarizing scatterers, N_D, and non-depolarizing scatterers, N_ND. Depolarization reaches a maximum for approximately 2 scatterers per volume. Non-depolarizing scattering biases the depolarization from GNRs and restores sensitivity (dynamic range) to higher GNR concentrations, preventing a premature depolarization maximum.

Spontaneous bilateral seizure with unilateral spreading depolarization and seizure independent spreading depolarization in Kcna1 KO mice. Chronic DC recording in juvenile K_v1.1/Kcna1 KO mice. (A) Representative trace of spreading depolarization following a seizure (postictal spreading depolarization, B) and isolated unilateral spreading depolarization (C). (D and E) EEG characteristics of spreading depolarizations. No clear EEG suppression was detected in these recordings. (F) Unlike Kcnq2-cKO mice, seizure (n = 166) and spreading depolarization (n = 14) were often detected independently, and a seizure + spreading depolarization (SD) complex accounted for 4.8% (9/189) of total events. (G) Histogram of seizure, spreading depolarization, and seizure + spreading depolarization detected from eight K_v1.1 KO mice. There was no clear circadian dependency.

Data obtained using the protocol shown in Fig. . (A) Scatter plot of ISI vs. PSP amplitude with minimal central depolarization of B21 (soma 10 mV above resting membrane potential) (blue circles) and with maximal central depolarization (soma 30 mV above resting membrane potential) (red squares). Note that facilitation is only observed with maximal central depolarization. (B) Bar graphs plotting the mean PSP amplitude at a short ISI (first bin of pooled data) vs. a long ISI (last bin) with minimal central depolarization (blue) and with maximal central depolarization (red). Note that there was no significant difference with minimal central depolarization, whereas there was a significant difference when B21 was maximally depolarized. (C) Scatter plot of normalized calcium fluorescence vs. PSP amplitude with minimal central depolarization of B21 (blue circles) and with maximal central depolarization (red squares). Note that there was no correlation between calcium fluorescence and PSP amplitude with minimal central depolarization. A correlation was however observed with maximal depolarization. In all cases data are plotted as means ± SEMs.

There was no evidence for distinct subgroups of corticocollicular neurons based on variability in intrinsic properties. A1, Input resistance was not different between corticocollicular neurons displaying broad depolarization (gray) and those without (black; R_i: narrow depolarization: 211.9 ± 22.6 MΩ, n = 23; broad depolarization = 184 ± 17.1 MΩ, n = 15; p = 0.32). A2, Resting membrane potential (V_m) was not different between corticocollicular neurons displaying and neurons not displaying broad depolarization (V_m: narrow depolarization = −63.1 ± 5.0 mV, n = 22; broad depolarization = −61.4 ± 4.4 mV, n = 15; p = 0.26). A3, AP width was not different between corticocollicular neurons displaying and neurons not displaying broad depolarization (AP width: narrow depolarization = 1.94 ± 0.33 ms, n = 8; broad depolarization = 1.75 ± 0.25 ms, n = 10; p = 0.08). A4, AP threshold was not different between corticocollicular neurons displaying and neurons not displaying broad depolarization (narrow depolarization = −44 ± 7.5 mV, n = 8; broad depolarization = −41.3 ± 5.8 mV, n = 10; p = 0.09). B1, Relationship of the variability of the amplitude of the narrow depolarization (first amp.) and R_i in corticocollicular neurons (narrow depolarization: R² = 0.55, n = 23, p = 0.007; broad depolarization: R² = 0.20, n = 13, p = 0.50). B2, Relationship of the variability of the amplitude of the narrow depolarization and V_m in corticocollicular neurons (narrow depolarization: R² = 0.10, n = 19, p = 0.68; broad depolarization: R² = 0.20, n = 13, p = 0.50). B3, Relationship of the variability of the amplitude of the narrow depolarization and AP width in corticocollicular neurons (narrow depolarization: R² = 0.27, n = 8, p = 0.57; broad depolarization: R² = 0.05, n = 10, p = 0.88). B4, Relationship of the variability of amplitude of the narrow depolarization and AP threshold in corticocollicular neurons (narrow depolarization: R² = 0.10, n = 8, p = 0.67; broad depolarization: R² = 0.41, n = 10, p = 0.28). C1, Relationship of the variability of the amplitude of the broad depolarization (second amp.) and Ri in corticocollicular neurons (broad depolarization: R² = 0.53, n = 13, p = 0.15). C2, Relationship of the variability of the amplitude of the broad depolarization and V_m in corticocollicular neurons (broad depolarization: R² = 0.46, n = 13, p = 0.12). C3, Relationship of the variability of the amplitude of the broad depolarization and AP width in corticocollicular neurons (broad depolarization: R² = 0.43, n = 10, p = 0.25). C4, Relationship of the variability of the amplitude of the broad depolarization and AP threshold in corticocollicular neurons (broad depolarization: R² = 0.38, n = 10, p = 0.31).