Fig. 3: DG lesions, but not MEC lesions substantially broaden the onset phase of CA3 spike trains. | Nature Communications

Fig. 3: DG lesions, but not MEC lesions substantially broaden the onset phase of CA3 spike trains.

From: Distinct roles of dentate gyrus and medial entorhinal cortex inputs for phase precession and temporal correlations in the hippocampal CA3 area

Fig. 3

a Onset and offset phases of spike trains from CA3 cells in control (CTRL(DG)) and DG-lesion rats (LESION(DG)). In each of the four raster plots, each row displays the onset phase (Φon) or offset phase (Φoff) of the trains of a cell (in gray), and the cell’s median onset or offset phase (light blue, control; dark blue, DG-lesion). Cells within each panel are sorted from top to bottom by their median onset/offset phase. Data are repeated from 2π to 4π for clarity, and two LFP theta cycles are displayed on top for reference. b The cells’ median onset and offset phases (shown in blue in panel a) were compared between control and DG-lesion rats. Data are repeated from 2π to 4π. Note the greater concentration of onset phases in the ascending (i.e., late) portion of the theta cycle in cells from control compared to DG-lesion rats. The distribution of onset phases differed between CTRL(DG) (light blue bars; n = 84 cells) and LESION(DG) groups (dark blue line; n = 68 cells, χ2 = 24.4, p = 5.0 × 10−6, circular MANOVA) with a higher concentration in the control group (phase concentration: CTRL(DG) κ = 1.91, LESION(DG) κ = 0.42, U = 25.8, p = 3.7 × 10−7, concentration test). Offset phases were not altered by the lesion (χ2 = 3.25, p = 0.20, circular MANOVA; phase concentration: CTRL(DG) κ = 0.80, LESION(DG) κ = 0.95, U = 0.32, p = 0.57, concentration test). c The dispersion of the phase of the first and last spikes was calculated across spike trains of each cell, and the cells’ dispersions were compared between control and DG-lesion rats. Dispersions of the cells’ onset phase but not of the cells’ offset phase increased with DG lesions (onset: z-statistic = − 4.11, p = 3.9 × 10−5; offset: z-statistic = − 1.33, p = 0.18, MW tests). The arrowheads mark the median circular variance values (control, light blue; lesion, dark blue). d–f, As (a–c), but for the cells from MEC-lesion rats (LESION(MEC)) and their corresponding controls (CTRL(MEC)). Onset phase values again peaked in the ascending phase of the theta cycle, but their distribution was not altered by the lesion (n = 101 CTRL(MEC) and 158 LESION(MEC) cells, χ2 = 1.18, p = 0.56, circular MANOVA; phase concentration: CTRL(MEC) κ = 1.49, LESION(MEC) κ = 1.33, U = 0.44, p = 0.51, concentration test). Similarly, the distribution of offset phases did not differ between cells of MEC-lesion and control rats (χ2 = 2.18, p = 0.34, circular MANOVA; concentration: CTRL(MEC) κ = 1.08, LESION(MEC) κ = 1.16, U = 0.15, p = 0.70, concentration test). Dispersions of onset and offset phases were moderately broadened by MEC lesions (onset: z-statistic = – 2.30, p = 0.021; offset: z-statistic = – 2.16, p = 0.031, MW tests), which is consistent with an overall increase in variability in theta phase preference. n.s., not significant, *** p < 0.001. Source data are provided as a Source Data file.

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