Molecular Indicators of Stress-Induced Neuroinflammation in a Mouse Model Simulating Features of Post-Traumatic Stress Disorder (Open Access)
Journal Article - Open Access
U.S Army Center for Environmental Health Research Fort Detrick United States
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A social-stress mouse model was used to simulate features of post-traumatic stress disorder PTSD. The model involved exposure of an intruder male C57BL6 mouse to a resident aggressor male SJL mouse for 5 or 10 consecutive days. Transcriptome changes in brain regions hippocampus, amygdala, medial prefrontal cortex and hemibrain, blood and spleen as well as epigenome changes in the hemibrain were assayed after 1- and 10-day intervals following the 5-day trauma or after 1- and 42-day intervals following the 10-day trauma. Analyses of differentially expressed genes common among brain, blood and spleen and differentially methylated promoter regions revealed that neurogenesis and synaptic plasticity pathways were activated during the early responses but were inhibited after the later post-trauma intervals. However, inflammatory pathways were activated throughout the observation periods, except in the amygdala in which they were inhibited only at the later post-trauma intervals. Phenotypically, inhibition of neurogenesis was corroborated by impaired Y-maze behavioral responses.