Blunted basal corticosterone pulsatility predicts post-exposure susceptibility to PTSD phenotype in rats

Danan, Dor; Matar, Michael A.; Kaplan, Zeev; Zohar, Joseph; Cohen, Hagit

doi:10.1016/j.psyneuen.2017.09.023

Cited by 31 publications

(21 citation statements)

References 47 publications

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“…Effects of PTSD on plasma corticosterone/cortisol have been studied on different PTSD models and in clinical studies. Some PTSD models induced an increase in plasma corticosterone, such as single and done-twice predator stress [ 10 , 11 ]. Furthermore, Wilson et al (2013) observed both elevated adrenal corticosterone production and adrenal gland hypertrophy [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

Hexobarbital Sleep Test for Predicting the Susceptibility or Resistance to Experimental Posttraumatic Stress Disorder

Komelkova

Манухина

Downey

et al. 2020

IJMS

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Hexobarbital sleep test (HST) was performed in male Wistar rats (hexobarbital 60 mg/kg, i.p.) 30 days prior to stress exposure. Based on the duration of hexobarbital-induced sleep, rats were divided into two groups, animals with high intensity (fast metabolizers (FM), sleep duration <15 min) or low intensity of hexobarbital metabolism (slow metabolizers (SM), sleep duration ≥15 min). The SM and FM groups were then divided into two subgroups: unstressed and stressed groups. The stressed subgroups were exposed to predator scent stress for 10 days followed by 15 days of rest. SM and FM rats from the unstressed group exhibited different behavioral and endocrinological patterns. SM showed greater anxiety and higher corticosterone levels. In stressed animals, anxiety-like posttraumatic stress disorder (PTSD) behavior was aggravated only in SM. Corticosterone levels in the stressed FM, PTSD-resistant rats, were lower than in unstressed SM. Thus, HST was able to predict the susceptibility or resistance to experimental PTSD, which was consistent with the changes in glucocorticoid metabolism.

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Section: Discussionmentioning

confidence: 99%

Hexobarbital Sleep Test for Predicting the Susceptibility or Resistance to Experimental Posttraumatic Stress Disorder

Komelkova

Манухина

Downey

et al. 2020

IJMS

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“…In both sexes, extreme behavioral response rats displayed inhibited cardiac autonomic system habituation and recovery after exposure 121 . Early life stress increased vulnerability to cardiac autonomic dysfunction, and blunted basal CORT pulse amplitude predicted post-exposure PTSD susceptibility 122,123 . Avoidance of bobcat urine-paired context predicted post-stress thermal hyperalgesia in Wistar rats with high stress reactivity 111 .…”

Section: Predator Stressmentioning

confidence: 99%

Rodent models of post-traumatic stress disorder: behavioral assessment

2020

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Although the etiology and expression of psychiatric disorders are complex, mammals show biologically preserved behavioral and neurobiological responses to valent stimuli which underlie the use of rodent models of post-traumatic stress disorder (PTSD). PTSD is a complex phenotype that is difficult to model in rodents because it is diagnosed by patient interview and influenced by both environmental and genetic factors. However, given that PTSD results from traumatic experiences, rodent models can simulate stress induction and disorder development. By manipulating stress type, intensity, duration, and frequency, preclinical models reflect core PTSD phenotypes, measured through various behavioral assays. Paradigms precipitate the disorder by applying physical, social, and psychological stressors individually or in combination. This review discusses the methods used to trigger and evaluate PTSD-like phenotypes. It highlights studies employing each stress model and evaluates their translational efficacies against DSM-5, validity criteria, and criteria proposed by Yehuda and Antelman's commentary in 1993. This is intended to aid in paradigm selection by informing readers about rodent models, their benefits to the clinical community, challenges associated with the translational models, and opportunities for future work. To inform PTSD model validity and relevance to human psychopathology, we propose that models incorporate behavioral test batteries, individual differences, sex differences, strain and stock differences, early life stress effects, biomarkers, stringent success criteria for drug development, Research Domain Criteria, technological advances, and cross-species comparisons. We conclude that, despite the challenges, animal studies will be pivotal to advances in understanding PTSD and the neurobiology of stress. Introduction Post-traumatic stress disorder (PTSD) is an incapacitating chronic disorder. With a 3.9% lifetime prevalence rate worldwide and a 6.4-7.8% rate in the USA, PTSD's health burden is substantial 1-5. Based on the World Mental Health Surveys, 69.7% worldwide (82.7% in the USA) reported exposure to a traumatic experience. While trauma exposure is a required criterion for PTSD diagnosis, only 5.6% worldwide (8.3% in the USA) of those who experienced trauma developed the disorder 1. This is due to numerous factors, including trauma type, variation in trauma response, social support, and endogenous factors of individuals. For adults, adolescents, and children older than six years, eight diagnostic criteria, defined in the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), specify measures concerning the victim's perception of trauma and symptoms. For children six years and younger, Criteria C and D (described below) are combined, making for seven diagnostic criteria 6. Criterion A: Exposure to actual or threatened death, serious injury, or sexual violence; one or more ways (e.g., direct experience, witnessing others, learning of close family member's or friend's trauma...

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“…Cinque et al (2017) reported that glucocorticoids levels were back to baseline values in both groups a few days after transfer and relocation. Danan (2018) also found that extreme disruption of behavior on day 8 post-exposure was also characterized by a blunting of corticosterone response to the stressor. Our results were consistent with the above results that chronic stress might reduce the sensitivity of HPA axis, and further droppings' corticosterone metabolites did not respond to changes in RH in the late period.…”

Section: Discussionmentioning

confidence: 82%

Effect of relative humidity at either acute or chronic moderate temperature on growth performance and droppings' corticosterone metabolites of broilers

Zhou

Zhang

et al. 2019

Journal of Integrative Agriculture

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The present study aimed to investigate the effect of relative humidity (RH) at either acute or chronic moderate ambient temperature (Ta) on growth performance and droppings' corticosterone metabolites of broilers. Two experiments were conducted: effect of RH (35, 60 or 85%) on average daily feed intake (ADFI) and droppings' corticosterone metabolites at acute (1 d: 20-26°C or 31-20°C, 26 or 31°C for 6 h d-1 at 10:00-16:00) moderate Ta (experiment 1) and effect of RH (35, 60 or 85%) on growth performance and droppings' corticosterone metabolites at chronic (step-wisely increasing temperature by 3°C every 3 d from 20 to 32°C within 15 d: 20-23-26-29-32°C) moderate Ta (experiment 2). Droppings were collected at the 2, 4, 6, 8, and 22 h after Ta-RH controlled in experiment 1 and at the 2, 4, 6, and 22 h after Ta controlled to 32°C in experiment 2. The results showed that: 1) In experiment 1, 85% RH increased (P<0.05) the droppings' corticosterone metabolites at the 2, 6, 8, and 22 h and 35% RH increased (P<0.05) it at the 2 and 22 h compared to the 60% RH. Moreover, 85% RH further increased (P<0.05) it compared to the 35% RH, however, no difference (P>0.05) was found in ADFI among the three RH groups at acute moderate 26°C; 35 and 85% RH increased (P<0.05) droppings' corticosterone metabolites at the 2, 6, 8 and 22 h and decreased (P<0.05) ADFI compared to the 60% RH, moreover, 85% RH further increased (P<0.05) droppings' corticosterone metabolites and further decreased (P<0.05) ADFI compared to the 35% RH at acute moderate 31°C; and the average of droppings' corticosterone metabolites in the whole period had a negative correlation (P<0.02) with the ADFI. 2) In experiment 2, 85% RH increased (P<0.01) droppings' corticosterone metabolites only at the 2 h and decreased (P<0.02) ADFI and average daily gain (ADG) compared to the 60% RH, no difference (P>0.05) in droppings' corticosterone metabolites was found between the 35 and 60% RH, however, 35% RH decreased (P<0.01) ADG compared to the 60% RH, and the average of droppings' corticosterone metabolites in the whole period also had a negative correlation (P<0.02) with ADFI and ADG. In conclusion, droppings' corticosterone metabolites could be used as a RH stress index and low and high RH, especially high RH, reduced growth performance possibly through inducing RH stress at moderate temperature.

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Blunted basal corticosterone pulsatility predicts post-exposure susceptibility to PTSD phenotype in rats

Cited by 31 publications

References 47 publications

Hexobarbital Sleep Test for Predicting the Susceptibility or Resistance to Experimental Posttraumatic Stress Disorder

Hexobarbital Sleep Test for Predicting the Susceptibility or Resistance to Experimental Posttraumatic Stress Disorder

Rodent models of post-traumatic stress disorder: behavioral assessment

Effect of relative humidity at either acute or chronic moderate temperature on growth performance and droppings' corticosterone metabolites of broilers

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