Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis

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.

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Rodent models of post-traumatic stress disorder: behavioral assessment.

Cortisol stress response in post-traumatic stress disorder, panic disorder, and major depressive disorder patients

Neurobiological systems may be particularly susceptible to deleterious impact of childhood trauma, and the impact of childhood trauma on development and subsequent functional outcomes across the lifespan has been well-documented The current review addresses the neurobiological impact of exposure to interpersonal trauma in childhood in the context of executive function, emotion regulation, and dissociation/interoceptive awareness Subsequent risk for PTSD and depression is also discussed The pathway of risk from childhood trauma to these cognitive, emotional, and psychiatric outcomes is addressed in terms of potential structural and functional alterations within the hippocampus, prefrontal cortex, and amygdala resulting from chronic or repeated activation of the hypothalamic-pituitary-adrenal (HPA) axis and its interaction with and influence on genetic and epigenetic processes during sensitive periods of development Implications for practice are discussed

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Neurobiological Development in the Context of Childhood Trauma.

https://researchsystem.canberra.edu.au/ws/files/27781737/1_s2.0_S2352289518301085_main.pdf

Katharina Köhler

Papers

Identification and characterization of HPA-axis reactivity endophenotypes in a cohort of female PTSD patients