Stress Controversies: Post‐Traumatic Stress Disorder, Hippocampal Volume, Gastroduodenal Ulceration *

  title={Stress Controversies: Post‐Traumatic Stress Disorder, Hippocampal Volume, Gastroduodenal Ulceration *},
  author={George Fink},
  journal={Journal of Neuroendocrinology},
  • G. Fink
  • Published 1 February 2011
  • Biology
  • Journal of Neuroendocrinology
Stress in mammals triggers a neuroendocrine response mediated by the hypothalamic–pituitary–adrenal axis and the autonomic nervous system. Increased activity of these two systems induces behavioural, cardiovascular, endocrine and metabolic cascades that enable the individual to fight or flee and cope with the stress. Our understanding of stress and stress‐response mechanisms is generally robust. Here, however, we review three themes that remain controversial and perhaps deserve further scrutiny… 

Stress risk factors and stress-related pathology: Neuroplasticity, epigenetics and endophenotypes

This paper highlights a symposium on stress risk factors and stress susceptibility, presented at the Neurobiology of Stress workshop in Boulder, CO, in June 2010, and highlighted emerging themes regarding the role of brain reorganization, individual differences, and epigenetics in determining stress plasticity and pathology.

Central Dopaminergic System and Its Implications in Stress-Mediated Neurological Disorders and Gastric Ulcers: Short Review

The literature survey suggests that dopaminergic system has received little attention in both clinical and preclinical research on stress, but the current research on this issue will surely identify a better understanding of stressful events and will give better ideas for further efficient antistress treatments.

Changes in integrin αv, vinculin and connexin43 in the medial prefrontal cortex in rats under single-prolonged stress

It is demonstrated that apoptotic cells significantly increased in the mPFC of SPS rats, accompanied with changes in expression of integrin αv, vinculin and connexin43, and the mitochondrial pathway were involved in the process of S PS-induced apoptosis.

Study of the variations in apoptotic factors in hippocampus of male rats with posttraumatic stress disorder

The activation of caspase-3 in the stress groups indicates that apoptosis may be one of the reasons inducing hippocampus atrophy and play roles in the pathogenesis of PTSD.

Top‐down and bottom‐up control of stress‐coping

This 30th anniversary issue review of glucocorticoid modulation of limbic‐prefrontocortical circuitry during stress‐coping highlights the involvement of adipose tissue in the allocation of energy resources to central regulation of stress reactions, and evaluates the role of cortisol as a pleiotropic regulator in vulnerability to, and treatment of, trauma‐related psychiatric disorders.

Glucocorticoids and the brain after critical illness.

The role of endogenous and exogenous glucocorticoids in neuropsychiatric outcomes following critical illness is examined and current evidence indicates that glucoc Corticoids during illness may protect against the development of post-traumatic stress disorder (PTSD).

Glucocorticoids and the Brain after Critical Illness

This review examines the role of endogenous and exogenous glucocorticoids in neuropsychiatric outcomes following critical illness and proposes future directions for research in this field, including determining therole of persistent glucOCorticoid elevations after illness in neuroPsychiatric outcomes.



Noradrenergic dysfunction and the psychopharmacology of posttraumatic stress disorder

Studies of central noreadrenergic hyperactivity under both basal and challenge conditions are reviewed and the evidence for these derangements as potential psychopharmacologic targets in patients with PTSD is explored.

Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders.

  • R. Sapolsky
  • Psychology, Biology
    Archives of general psychiatry
  • 2000
This review examines the evidence for hippocampal atrophy in Cushing syndrome, which is characterized by a pathologic oversecretion of glucocorticoids; (2) episodes of repeated and severe major depression; (3) posttraumatic stress disorder and what cellular mechanisms underlie the overall decreases in hippocampal volume.

Glucocorticoids, depression, and mood disorders: structural remodeling in the brain.

  • B. McEwen
  • Psychology, Biology
    Metabolism: clinical and experimental
  • 2005

Biology of Post‐Traumatic Stress Disorder in Childhood and Adolescence

  • P. Pervanidou
  • Psychology, Biology
    Journal of neuroendocrinology
  • 2008
It is hypothesised that, in adults with chronic PTSD, low cortisol levels, together with high catecholamines, may reflect a late event in the natural history of the disorder, months or years after the trauma.

Autonomic and Respiratory Characteristics of Posttraumatic Stress Disorder and Panic Disorder

Several psychophysiological measures exhibited group-comparison effect sizes in the order of 1.0, supporting their potential for enhancing differential diagnosis and possibly suggesting utility as endophenotypes in genetic studies of anxiety disorders.

Cardiovascular manifestations of posttraumatic stress disorder.

  • U. BediR. Arora
  • Psychology, Biology
    Journal of the National Medical Association
  • 2007
The effects of PTSD on the cardiovascular system are discussed, which states that chronic stressors over long durations of time lead to increased neuroendocrine responses, which have adverse effects on the body.