Extended Data Figure 9: Phase-locking of individual neurons to the 20–40-Hz rhythm. | Nature

Extended Data Figure 9: Phase-locking of individual neurons to the 20–40-Hz rhythm.

From: Coordination of entorhinal–hippocampal ensemble activity during associative learning

Extended Data Figure 9

a, Raster plots showing cue-port activity of example dCA1 cell on successive trials at T5. Rows correspond to individual trials; ticks indicate spikes. Top, trials with food in left cup; middle, trials with food in right cup; bottom, peri-stimulus time histogram (PSTH); orange, left-predicting trials; black, right-predicting trials. Between T1 and T5, the number of dCA1 cells with mean rates above 1 Hz during the cue interval ranged from 63 to 75 (5 rats). b, Spike-time distribution for dCA1 principal cells with cue-port activity across phase of local 20–40-Hz oscillation at T1–T5 and T5e. c, d, Percentage of significantly phase-locked cells (c) and mean vector length of distribution in b (d), averaged across dCA1 cells with cue-port activity. T5d as in Fig. 2c. *#, as in Fig. 2c. eh, LEC cells, as in ad. Between T1 and T5, the number of LEC cells with mean rates above 1 Hz during the cue interval ranged from 76 to 82 (5 rats). The number of cue-port cells phase-locked to the local 20–40-Hz LFP increased significantly from T1 to T5 in both dCA1 and LEC (main text) and there was a significant increase in the phase locking of each cell (ANOVA for mean vector length: dCA1: F(4, 348) = 2.81, P = 0.026; LEC: F(4, 383) = 21.0, P < 0.001). On error trials, the mean vector for the spike-phase distribution decreased in both dCA1 and LEC (dCA1: two-tailed paired t-test, t(72) = 2.97, P = 0.004; LEC: t(81) = 4.05, P < 0.001). i, j, Interregional phase-locking of individual dCA1 and LEC cells. i, Phase-locking of dCA1 spikes as shown in c and d, but against 20?40-Hz oscillations in LEC. Left, percentage of significantly phase-locked cells. Right, mean vector length of the spike-phase distribution. The percentage of cells that was significantly phase-locked to the oscillations increased from 7.9 at T1 to 17.4 at T5 (P < 0.005; binomial test with Bonferroni correction). This increase was matched by an increase in the mean vector length of the spike-phase distribution (ANOVA for mean vector length: F(4, 348) = 2.8, P = 0.03). T5e and T5d indicate T5 error trials and down-sampled correct T5 trials, respectively. Mean vector length on T5e was significantly reduced compared to T5d (two-tailed paired t-test, t(72) = 2.60, P = 0.011). j, Phase-locking of LEC spikes as shown in g and h, but against 20–40-Hz oscillations in dCA1. The percentage of LEC cells significantly phase-locked to 20–40-Hz oscillations in dCA1 increased from 13.3 at T1 to 24.4 at T5 (P < 0.005). This was accompanied by a significant increase in the mean vector length of the spike-phase distribution (F(4, 383) = 2.7, P = 0.03). Mean vector length on error trials (T5e) decreased significantly compared to down-sampled correct trials (T5d; two-tailed paired t-test, t(81) = 2.42, P = 0.017). *P < 0.05, Bonferroni post-hoc test; #P < 0.05, paired t-test.

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