Biddle, Matthew2022-10-272022-10-272022https://udspace.udel.edu/handle/19716/31534Post traumatic stress disorder (PTSD) is a debilitating psychiatric disorder which stems from fear memory persistence after exposure to a traumatic experience. PTSD is associated with a high socioeconomic cost, as well as a higher prevalence rate in women than in men, though the reason behind this sex difference remains unknown. A possible explanation may be cyclic changes in vascular estrogen release, which may be a contributing factor to the higher prevalence of PTSD, though the role of estrogen receptors in modulating traumatic stress effects has been insufficiently explored. By using a well-validated PTSD model (single prolonged stress – SPS) in female rats, we first studied the effects of antagonizing nuclear estrogen receptors (Experiment 1), finding that SPS induced persistent fear memory (measured using freezing) and that this response was not affected by antagonism of nuclear estrogen receptors. Following this, we examined the effects of agonizing G-protein coupled estrogen receptors (GPERs, Experiment 2), finding that SPS had no effect on persistent fear memory, and that activation of GPERs prior to SPS had no effect on persistent fear memory. Finally, we studied the effects of activating estrogen receptors utilizing 17β-estradiol, and found that SPS increased persistent fear memory (measured using darting), and that this enhancement in persistent fear memory was attenuated by activation of estrogen receptors prior to SPS. Overall, the results of the study suggest that SPS effects on persistent fear memory can be observed in female rats (by measuring multiple behaviors) and that increasing estrogen levels prior to SPS attenuates persistent fear memory induced by SPS in female rats.Fear memoryEstrogen receptorsTraumatic stressThesis13489470832022-08-10en