Abstract
People with post-traumatic stress disorder (PTSD) exhibit heightened anxiety and enhanced negative feedback of the hypothalamus-pituitary-adrenal (HPA) axis. We previously reported that male rats exposed to a predator-based psychosocial stress model of PTSD exhibited comparable changes in anxiety-like behavior and HPA axis activity, including lower baseline levels of corticosterone and a greater suppression of corticosterone after dexamethasone administration. Here, we assessed whether we would observe similar effects in female rats exposed to this model. Adult female Sprague-Dawley rats were exposed to a cat on two occasions (separated by 10 days), in combination with chronic social instability. Three weeks after the second cat exposure, we assessed anxiety-like behavior on an elevated plus maze (EPM) and collected blood samples from rats in the absence or presence of dexamethasone to quantify serum corticosterone levels. Although stressed females did not display heightened anxiety on the EPM, they exhibited significantly lower overall corticosterone levels and a greater suppression of corticosterone after dexamethasone administration. The observation of significantly lower overall corticosterone levels in stressed females was replicated in a separate, independent experiment. These findings suggest that the predator-based psychosocial stress model of PTSD may be useful for studying mechanisms that underlie changes in HPA axis function in females exposed to trauma.
Highlights
Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition characterized by heightened anxiety, hyperarousal, intrusive memories, cognitive impairments, and several deleterious physiological symptoms (Zoladz and Diamond, 2013)
We examined whether this model of post-traumatic stress disorder (PTSD) would produce the same PTSDlike glucocorticoid abnormalities in females that were previously observed in males
The Stress × Time Point interaction was not significant, [F(2, 60) = 2.51, p = 0.09], we performed Bonferroni-corrected comparisons to examine corticosterone levels between stressed and non-stressed females at each time point. These comparisons revealed that stressed females exhibited significantly lower corticosterone levels than non-stressed females following 20 min of immobilization, t(30) = 2.79, corrected p = 0.009, but not at baseline, t(30) = 1.29, corrected p = 0.206, or an hour following the termination of immobilization, t(30) = 1.10, corrected p = 0.280
Summary
Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition characterized by heightened anxiety, hyperarousal, intrusive memories, cognitive impairments, and several deleterious physiological symptoms (Zoladz and Diamond, 2013). Findings have been mixed (Meewisse et al, 2007; Speer et al, 2019), research has generally shown that people with PTSD display abnormally low levels of cortisol, a greater suppression of cortisol following dexamethasone administration, and increased glucocorticoid receptor sensitivity (Lehrner et al, 2016) These HPA axis alterations might exist prior to PTSD onset and Glucocorticoid Abnormalities in Stressed Females confer increased risk for the disorder or reflect the pathophysiology of trauma- and/or PTSD-related symptoms. The model was explicitly designed to incorporate features that are known to be associated with increased susceptibility for PTSD in traumatized individuals (Zoladz et al, 2015) It consists of a 31-day paradigm, during which rats are exposed to an adult, female cat (i.e., predator stress) on two occasions (separated by 10 days) and experience chronic social instability by having their cage mates changed daily (Zoladz et al, 2008). We examined whether this model of PTSD would produce the same PTSDlike glucocorticoid abnormalities in females that were previously observed in males
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