The DMN is one of the most consistently identified RSNs, anchored in a midline core consisting of two key hub structures, the posterior cingulate cortex (PCC) and the medial prefrontal cortex (mPFC; Buckner et al., 2008; Yeo et al., 2011). While prominent in the resting state, the DMN is deactivated by salient sensory input or externally-oriented cognitive processing and, accordingly, exhibits reciprocal inhibition with neural networks associated with these processes (Gusnard et al., 2001; Raichle et al., 2001; Greicius et al., 2003; Greicius and Menon, 2004). As such, DMN dysfunctions can interrupt internal mentation or ‘tranquil’ resting states and heighten vigilance and attention. Indeed, DMN dysfunction has been linked to heightened acute stress response (Menon, 2011; Hermans et al., 2014; Zhang et al., 2019) and implicated in PTSD symptoms of hypervigilance and negative intrusions (Abdallah et al., 2017; Akiki et al., 2018).
