Psychosocial animal model of PTSD produces a long-lasting traumatic memory, an increase in general anxiety and PTSD-like glucocorticoid abnormalities

• Published in: Psychoneuroendocrinology 2012-09, Vol.37 (9), p.1531-1545
• Main Authors: Zoladz, Phillip R, Fleshner, Monika, Diamond, David M
• Format: Article
• Language: English
• Subjects: Adult and adolescent clinical studies; Animal model; Animal models; Animals; Anxiety; Anxiety - physiopathology; Anxiety - psychology; Anxiety disorders. Neuroses; Behavioral psychophysiology; Biological and medical sciences; Cats; Cognition; Complications; Dexamethasone; Disease Models, Animal; Endocrinology & Metabolism; Exploratory Behavior - physiology; Fear; Fear - physiology; Fear conditioning; Fundamental and applied biological sciences. Psychology; Glucocorticoids; Glucocorticoids - blood; Hormones and behavior; HPA axis; Hypothalamo-Hypophyseal System - physiopathology; Male; Medical sciences; Memory; Memory - physiology; Motor Activity - physiology; Neuroendocrine system; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System - physiopathology; Post-traumatic stress disorder; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychopathology. Psychiatry; Rats; Rats, Sprague-Dawley; Social interactions; Stress; Stress Disorders, Post-Traumatic - physiopathology; Stress Disorders, Post-Traumatic - psychology; Trauma
• ISSN: 0306-4530; 1873-3360
• DOI: 10.1016/j.psyneuen.2012.02.007

Summary 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.