期刊
PSYCHONEUROENDOCRINOLOGY
卷 37, 期 9, 页码 1531-1545出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2012.02.007
关键词
Stress; Trauma; Glucocorticoids; HPA axis; Memory; Dexamethasone; Animal model; Fear conditioning
资金
- Department of Veterans Affairs
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. (C) 2012 Elsevier Ltd. All rights reserved.
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