Accession Number : ADA622595


Title :   Brain Transcriptome Profiles in Mouse Model Simulating Features of Post-traumatic Stress Disorder


Descriptive Note : Journal article


Corporate Author : ARMY CENTER FOR ENVIRONMENTAL HEALTH RESEARCH FORT DETRICK MD


Personal Author(s) : Muhie, Seid ; Gautam, Aarti ; Meyerhoff, James ; Chakraborty, Nabarun ; Hammamieh, Rasha ; Jett, Marti


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/a622595.pdf


Report Date : 28 Feb 2015


Pagination or Media Count : 23


Abstract : Social-stress mouse model, based on the resident-intruder paradigm was used to simulate features of human post-traumatic stress disorder (PTSD). The model involved exposure of an intruder (subject)mouse to a resident aggressor mouse followed by exposure to trauma reminders with rest periods. C57BL/6 mice exposed to SJL aggressor mice exhibited behaviors suggested as PTSD-in-mouse phenotypes: intermittent freezing, reduced locomotion, avoidance of the aggressor-associated cue and apparent startled jumping. Brain tissues (amygdala,hippocampus, medial prefrontal cortex, septal region, corpus striatum and ventral striatum) from subject (aggressor exposed: Agg-E) and control C57BL/6 mice were collected at one, 10 and 42 days post aggressor exposure sessions. Transcripts in these brain regions were assayed using Agilent's mouse genome-wide arrays. Results: Pathways and biological processes associated with differentially regulated genes were mainly those thought to be involved in fear-related behavioral responses and neuronal signaling. Expression-based assessments of activation patterns showed increased activations of pathways related to anxiety disorders (hyperactivity and fear responses), impaired cognition, mood disorders, circadian rhythm disruption, and impaired territorial and aggressive behaviors. In amygdala, activations of these pathways were more pronounced at earlier time-points, with some attenuation after longer rest periods. In hippocampus and medial prefrontal cortex, activation patterns were observed at later time points. Signaling pathways associated with PTSD-comorbid conditions, such as diabetes, metabolic disorder, inflammation and cardiac infarction, were also significantly enriched. In contrast, signaling processes related to neurogenesis and synaptic plasticity were inhibited.


Descriptors :   *POST TRAUMATIC STRESS DISORDER , ASSAYING , BEHAVIOR , BRAIN , CIRCADIAN RHYTHMS , CLINICAL MEDICINE , ELECTROPHYSIOLOGY , EXPOSURE(PHYSIOLOGY) , FEAR , GENOME , HEART , HIPPOCAMPUS , INFARCTION , INFLAMMATION , LOCOMOTION , MENTAL DISORDERS , METABOLIC DISEASES , MICE , MORBIDITY , NERVE CELLS , NEUROLOGY , PHYSIOLOGICAL EFFECTS , PROTEINS , RESPONSE(BIOLOGY) , SIGNS AND SYMPTOMS , SYNAPSE , TISSUES(BIOLOGY) , TRANSCRIPTION(GENETICS) , TRAUMA


Subject Categories : Psychology
      Biochemistry
      Medicine and Medical Research
      Stress Physiology


Distribution Statement : APPROVED FOR PUBLIC RELEASE