sensory (visual) cortex and between the VC and DMN hubs (Scheeringa et al., 2012). While this protective inhibitory process withstood the increased visual input at M-RS in the control group, it broke down among patients with PTSD, suggesting impaired gating of sensory entry to (i.e., compromised protection of) the DMN. Exploratory correlation analyses further indicated a close correlation between VC→PCC and PCC→mPFC α connectivity at M-RS (r = 0.31, p = 0.013), highlighting a mechanistic link between these two pathways. That is, disinhibited visual cortical propagation to the PCC, in the presence of strong environmental input, could further impair PCC-driven α synchronization with the mPFC, worsening DMN dysfunction in PTSD. Finally, to rule out the alternative explanation that emotional content (beyond visual stimulation) could contribute to the M-RS effects, we compared RS EEG data acquired before and after 5-min presentation of negative international affective picture system (IAPS) pictures from an independent sample of healthy individuals (N = 45). There was no change in α GC (t = 0.032, p = 0.974), suggesting that in the absence of visual stimulation, simple affective effects would not result in α connectivity change. Nonetheless, we cannot fully exclude the combined effects of emotion and
