In post-traumatic stress disorder (PTSD), individuals experience intrusive memories of trauma accompanied by hyperarousal and stress dysregulation. Treatments for PTSD are largely ineffective, representing an enormous area of unmet need. PTSD is differentiated from acute stress disorder (ASD) by the duration of symptom presentation; more or less than one month, respectively. Further, while nearly everyone experiences at least one traumatic event in their lifetime, only a subset develop PTSD. Taken together, this makes a strong argument for the importance of mechanistic research efforts aimed at incorporating the persistent nature of traumatic memories into their design, as well as variance in susceptibility.

To this end, we adapted a stress-enhanced fear memory (SEFM) protocol [1] to induce long-lasting, PTSD-like behaviors and molecular changes in mice with differential susceptibility to the stressor [2]. We used this protocol to investigate molecular pathways supporting persistent stress susceptibility versus resilience, focusing on the basolateral amygdala (BLA), an “emotional” memory center of the brain that is hyperactive in PTSD. First, we reported a transcriptional profile in the BLA associated with susceptibility that included differential expression of genes with known polymorphisms in PTSD subjects present for at least one month after SEFM training [2].

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