Biophysical mechanisms of default mode network function and dysfunction
Trang-Anh E. Nghiem, Vinod Menon preprint
Stimulating the insula node of the salience network suppresses default mode network (DMN) activity in computational simulations, while cingulate cortex stimulation enhances retrosplenial cortex activity. Prelimbic cortex stimulation partially replicates insula-mediated suppression but fails to suppress cingulate regions, suggesting it acts as a functional bridge between networks. DMN emergence as a functionally segregated network is robust across wide ranges of excitatory-inhibitory balance and cholinergic modulation, but outside these boundaries, integrity breaks down through three failure modes: loss of responsiveness, reversal of suppression to enhancement, and network fragmentation.