Figure 11. The change in the intraburst spike rate in VSI correlated with the extent of polysynaptic actions induced by combined action of C2 and DSI. A, Simultaneous intracellular recordings from C2, DSI, and VSI from two representative animals (animals X and Y). Five minutes after cutting PdN6, animal X showed a decrease in the number of VSI spikes during the second burst of the swim motor pattern (asterisk). In contrast, there was little effect on the spiking in the second VSI burst in animal Y (asterisk). Twenty-two hours after PdN6 cut, VSI spiking during the second burst of the swim motor pattern recovered in animal X (arrowhead), whereas 19 h after PdN6 the VSI in animal Y fired fewer spikes than before (arrowhead). Arrows (Stim) indicate the time of PdN3 stimulation. B–D, Bar graphs show the average number of spikes of C2 (B), DSI (C), and VSI (D) in the second burst in the swim motor pattern counted before cutting PdN6 (Intact), shortly after cutting PdN6 (<1 h), and the next day (10–30 h). Before cutting PdN6, the number of spikes in the second bursts were 50.4 ± 16.0 (C2, N = 45), 34.8 ± 9.8 (DSI, N = 41), and 37.5 ± 8.8 (VSI, N = 45). Shortly after the cut (<1 h), they were 44.0 ± 15.4 (C2, N = 43), 32.7 ± 12.0 (DSI, N = 39), and 16.5 ± 12.0 (VSI, N = 47). The next day (10–30 h), they became 49.3 ± 20.5 (C2, N = 36), 36.5 ± 12.3 (DSI, N = 30), and 19.5 ± 12.9 (VSI, N = 41). The average number of VSI spikes shortly after cutting PdN6 and the next day were significantly lower than before the cut, as indicated by asterisks (p < 0.001 by Kruskal–Wallis one-way ANOVA on ranks with Dunn’s method). E–G, Plots of CoV corresponding to the bar graphs above (B–D). C2 and DSI showed relatively constant variance throughout the experiments (E, F), whereas VSI showed an increase in variance (G). There was a significant difference in variance of the VSI spike number between intact and <1 h (p = 0.02 by Levene median test) and between intact and 10–30 h (p = 0.002 by Levene median test). H, C2-evoked direct synaptic responses in VSI showed no correlation with the changes in the number of VSI spikes in the second burst of swim motor patterns. Changes in the number of VSI spikes in the second burst of motor patterns 15–30 h after PdN6 disconnection (ΔVSI spikes) were plotted against the change in the amplitudes of the depolarization phase of the C2+DSI-evoked synaptic potential measured (ΔVSI depolarization, Hi) or that of the C2+DSI-evoked hyperpolarization phase (Δhyperpolarization, Hii) in Hi-Di saline. There was no correlation between these parameters (p = 0.78 and 0.57, N = 14). I, The changes in the intraburst VSI spikes (ΔVSI spikes) upon recovery showed a significant correlation with the changes in the polysynaptic depolarization in VSI evoked by C2+DSI stimulation in normal saline (R
2 = 0.28, p = 0.004 by linear regression, N = 27). J, The changes in the number of VSI spikes in the second burst upon recovery was correlated with the changes in the frequency of small EPSPs recruited by C2+DSI stimulation (R
2 = 0.63, p < 0.001 by linear regression, N = 20).