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Resting state network (RSN) is a correlated activity of many neural structures in absence of external stimulation or functional tasks, and it is a fundamental endogenous feature of human and animal brain. The nature of this spontaneous activity remains poorly understood. According to our hypothesis it reflects hidden replay of neural networks of prior experience. We started a project on mouse cellular brain imaging that relates RSNs activity to animal’s past experiences. We characterized activity of 104 mouse brain areas and showed that RSNs identified by c-Fos protein were stable and reproducible. c-Fos activity of 42 selected brain areas was further investigated in naive and stressed mice that received post-traumatic stress disorder (PTSD) induction. Using Pearson correlation we reconstructed 7 networks with CCorr varying from 0.6 to 0.9 (inclusive, step=0.05) for naive and PTSD mice and compared experimentally identified networks with model networks (random, scale free and small world) of the same size using clustering, global efficiency and degree distribution. In both groups of mice, clustering was at the level of a random network. These clusters had weak interactions with each other: global efficiency of experimental networks was extremely low. PTSD induction strongly affected RSN activity all over the brain: PTSD RSN network was less clustered and clusters were separated by longer routes than in naive mice. PTSD induction caused global changes in the RSN structure: while in control animals cortical connectivity was high, in PTSD mice subcortical thalamus, striatum and amygdala were most connected. While cingulate and retrosplenial cortices were the main hubs in naive mice, functional connectivity between those areas was lost in PTSD mice, and paraventricular thalamus became a hub. Thus, we showed that experience of stressful event can change resting state network functional connectivity patterns long after the traumatic episode. Supported by RSF 16-15-00300.