The Role of Glucocorticoid Binding During Fear Conditioning in SPS-Induced Extinction Retention Defecits

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University of Delaware
Single prolonged stress (SPS) is a rat model of post-traumatic stress disorder (PTSD) that mimics several symptoms of the disease in humans. Rats that are exposed to SPS typically have significant extinction retention deficits and upregulation of glucocorticoid receptors (GRs) in the hippocampus. A causal relationship between these two effects has not been established. It is possible that increased GR binding during fear conditioning is responsible for extinction retention deficits seen in this model. In order to test this hypothesis, the glucocorticoid synthesis inhibitor metyrapone was administered 90 minutes before fear conditioning. SPS rats showed higher levels of freezing during fear conditioning and failed to acquire the extinction memory at the same rate as controls. SPS rats froze more during the extinction test as well. The 25mg/kgThere was no significant GR upregulation in any group. These data show that GR upregulation does not have a causal relationship with SPS-induced extinction retention deficits. It is possible that GR upregulation in SPS is protective, but this study does not provide evidence that GR upregulation plays a role in extinction learning.
Neuroscience, Brain Science, Psychology, Post-traumatic stress disorder