Shifting priorities: highly conserved behavioral and brain network adaptations to chronic stress across species.

摘要: Parallel clinical and preclinical research have begun to illuminate the biological basis of stress-related disorders, including major depression, but translational bridges informing discrete mechanistic targets for intervention are missing. To address this critical need, we used structural MRI in a mouse model large human sample examine stress effects on brain structure that may be conserved across species. Specifically, focused previously unexplored approach, whole-brain covariance, as it reflects synchronized changes neuroanatomy, potentially due mutual trophic influences or shared plasticity regions. Using unpredictable chronic mild (UCMS) paradigm first demonstrate UCMS-induced elevated behavioral emotionality correlates with increased size amygdala other corticolimbic We further identify focal increases amygdala’s ‘hubness’ (degree strength) set against background global loss network clustering modularity. These macroscopic supported molecular level by postsynaptic density-95 protein amygdala, consistent stress-induced plastic synaptic strengthening. Finally, provide evidence strikingly similar reorganization patterns exist young adults reporting high childhood trauma mood symptoms. Collectively, initial increase amygdala-centered synchrony, measured enhanced which is paralleled decrease synchrony. This putative trade-off reflected at expense dedifferentiation represent pathway depression related psychopathology.