Fig. 2. TG-PAC.

a, Average normalized modulation indices for all phase–amplitude pairs. n = 1,917 channels. b, The proportion of channels with significant theta–high-gamma PAC in each area, determined by comparisons to trial-shuffled surrogates (both loads). The horizontal lines indicate the 99th percentile of the surrogate null distribution per area (P = 0.005 for hippocampus (hippo.), amygdala (amy.) and vmPFC; right-sided permutation test, no adjustment for multiple comparisons). c, log-normalized modulation indices were averaged within the theta–high-gamma band in each load and compared between the loads in each significant PAC channel in each region. Only in the hippocampus, theta–high-gamma PAC differed as a function of load, with PAC higher in load 1 versus load 3 trials (left: n = 137 channels, P = 0.0005; amygdala (middle): n = 130, P = 0.38; vmPFC (right): n = 40, P = 0.87; two-sided permutation-based t-tests; FDR corrected for all five brain areas). z-scored values were shifted into a positive range by an offset of 1 and log-transformed for illustrative purposes only. All statistics are based on non-transformed z values. d, Example gamma amplitude distribution over theta phase as well as comodulograms with raw modulation indices in each load for a representative hippocampal channel. Note the wider distribution of gamma amplitude over theta phase in load 3 trials, which leads to lower levels of PAC (further analysis is provided in Extended Data Fig. 3a). Normalized MI values were as follows for the two examples shown: load 1, z = 16.52; load 3, z = 7.92. e, Average normalized modulation indices for significant hippocampal PAC channels. n = 137. f, TG-PAC was significantly negatively correlated with RTs in the hippocampus (n = 137, P = 6 × 10⁻⁵, mixed-effects GLM), but not in the amygdala (n = 130, P = 0.48) or the vmPFC (n = 40, P = 0.24). GLM results are shown in Supplementary Table 2. Each dot represents a significant PAC channel. For c,f, data are mean ± s.e.m. *P < 0.05; NS, not significant.