Post-traumatic stress disorder (PTSD) is characterized by a pathologically intense
memory for a traumatic experience, persistent anxiety and physiological abnormalities, such as
low baseline glucocorticoid levels and increased sensitivity to dexamethasone. We have
addressed the hypothesis that rats subjected to chronic psychosocial stress would exhibit
PTSD-like sequelae, including traumatic memory expression, increased anxiety and abnormal
glucocorticoid responses. Adult male Sprague-Dawley rats were exposed to a cat on two occasions
separated by 10 days, in conjunction with chronic social instability. Three weeks after the second
cat exposure, the rats were tested for glucocorticoid abnormalities, general anxiety and their
fear-conditioned memory of the two cat exposures. Stressed rats exhibited reduced basal
glucocorticoid levels, increased glucocorticoid suppression following dexamethasone administration,
heightened anxiety and a robust fear memory in response to cues that were paired with
the two cat exposures. The commonalities in endocrine and behavioral measures between
psychosocially stressed rats and traumatized people with PTSD provide the opportunity to
explore mechanisms underlying psychological trauma-induced changes in neuroendocrine systems
and cognition.