Mentor: Jennifer Quinn, Ph.D.

Post traumatic stress disorder (PTSD) is a mental health condition that is caused by an extremely stressful or traumatic event. In recent years fear research has been utilized to better understand how PTSD manifests within the brain. Several studies show that mu opioid receptors are linked to fear learning. There are a large number of these receptors in the amygdala, a brain region critical for fear. We and others have shown that exposure to early adversity leads to increased fear learning in adulthood. In this study, we will address whether this “stress-enhanced fear learning” (i.e., SEFL) is mediated by how rodents mu opioid receptors in the amygdala. We will use a genetically modified line of mice that have these receptors knocked out in the amygdala (i.e., MOR-KO) and control mice. Mice will be exposed to acute early life stress (aELS) or control (no-aELS) in infancy and then undergo fear conditioning and testing in adulthood. We hypothesize that the SEFL observed in previously-stressed animals is mediated by an increase in mu-opioid receptor expression in the amygdala. Thus, knockout of these receptors should eliminate SEFL in mice previously exposed to aELS.

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