Effects of chronic plus acute prolonged stress on measures of coping style, anxiety, and evoked HPA-axis reactivity

Abstract

Exposure to psychological trauma is the precipitating factor for PTSD. In addition, a history of chronic or traumatic stress exposure is a predisposing risk factor. We have developed a Chronic plus Acute Prolonged Stress (CAPS) treatment for rats that models some of the characteristics of stressful events that can lead to PTSD in humans. We have previously shown that CAPS enhances acute fear responses and impairs extinction of conditioned fear. Further, CAPS reduced the expression of glucocorticoid receptors in the medial prefrontal cortex. In this study we examined the effects of CAPS exposure on behavioral stress coping style, anxiety-like behaviors, and acute stress reactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Male Sprague-Dawley rats were exposed to CAPS treatment, consisting of chronic intermittent cold stress (4°C, 6hrs/day, 14 days) followed on day 15 by a single 1-hr session of sequential acute stressors (social defeat, immobilization, swim). After CAPS or control treatment, different groups were tested for shock probe defensive burying, novelty suppressed feeding, or evoked activation of adrenocorticotropic hormone (ACTH) and corticosterone release by an acute immobilization stress. CAPS resulted in a decrease in active burying behavior and an increase in immobility in the shock probe test. Further, CAPS-treated rats displayed increases in the latency to feed in the novelty suppressed feeding test, despite an increase in food intake in the home cage. CAPS treatment also reduced the HPA response to a subsequent acute immobilization stress. These results further validate CAPS treatment as a rat model of relevance to PTSD, and together with results reported previously, suggest that CAPS impairs fear extinction, shifts coping behavior from an active to a more passive strategy, increases anxiety, and alters HPA reactivity, resembling many aspects of human PTSD.

L-Tetrahydropalmatine Ameliorates Development of Anxiety and Depression-Related Symptoms Induced by Single Prolonged Stress in Rats

“…Many studies have shown that, consistent with PTSD models, SPS increased serum CORT concentrations, and decreased the sucrose preference of rats (Kozlovsky et al ., 2009; Roth et al ., 2012; Meyer et al ., 2013). Accordingly, the forced maintenance of high CORT levels and the decrease in sucrose preference associated with animal models can affect anxiety- and depression-like symptoms under experimental conditions, and this may be related to the progression or exacerbation of PTSD in humans (Serova et al ., 2013a).…”

Role of TrkB in the anxiolytic-like and antidepressant-like effects of vagal nerve stimulation: Comparison with desipramine

“…The NSFT was performed on Day 10 (see Figures 1A and 1B) and carried out as originally described by Bodnoff et al (1988) and by us previously (Furmaga et al, 2011, Roth et al, 2012). Rats were food deprived for 24 or 48 h prior to testing.…”

Depression, anxiety-like behavior and memory impairment are associated with increased oxidative stress and inflammation in a rat model of social stress

“…Although there exists large body of evidence demonstrating the negative impact of stress on emotional symptoms including depression, anxiety (Millan et al, 2012) and cognitive impairment (Alzoubi et al, 2013a; Devilbiss et al, 2012; Jonsdottir et al, 2013; Ohman et al, 2007; Ronnlund et al, 2013; Schwabe et al, 2012), however, studies investigating role of stress in comorbid prevalence of anxiety, depression and cognitive impairment in humans (Andreotti et al, 2013; Millan et al, 2012), or co-occurrence of anxiety and depression-like behaviors as well as learning-memory impairment, in animals are limited (Gomez et al, 2013; Haridas et al, 2013). Although impressive mechanistic insights have been offered by several groups, with regards to co-occurrence of anxiety-and depression-like behaviors in animal models (Mineur et al, 2013; Roth et al, 2012; Venzala et al, 2012), studies addressing the underlying biology of stress-induced co-occurrence of depression, anxiety and cognitive impairment are scarce.…”