Transcriptional changes across tissue and time provide molecular insights into a therapeutic window of opportunity following traumatic stress exposure

Survivors of traumatic stress exposure (TSE) frequently develop adverse posttraumatic neuropsychiatric sequelae (APNS) such as chronic pain and stress/depressive symptoms. Increasing evidence indicates that there is a window of opportunity following TSE in which therapeutic interventions are most effective against APNS, yet mechanisms accounting for this observation are poorly understood. We aimed to better understand such mechanisms by generating snapshots of the transcriptional landscape in the early aftermath of TSE across tissues and time. Adult Sprague Dawley rats were exposed to a TSE model, single prolonged stress (SPS). Then, eight tissues (hypothalamus, left and right hippocampus, amygdala, dorsal root ganglia, spinal cord, heart, and muscle) were isolated from these animals at 2, 24, and 72 hours after SPS and in unexposed controls (n=6 per group). This dataset includes raw deep sequencing transcript reads from each tissue at each study timepoint.