Glucocorticoids, a group of hormones that includes cortisol, are considered stress hormones because their levels increase following stress. When their relationship to stress was first identified, it was shown that the release of cortisol prepared the body to cope with the physical demands of stress.
Subsequently, high levels of cortisol were linked to depression and other stress-related disorders, giving rise to the hypothesis that high levels of cortisol on a long-term basis may impair the psychological capacity to cope with stress.
For this reason, drugs such as mifepristone that block glucocorticoid activity, called glucocorticoid receptor antagonists, have been tested as treatments for depression. But other recent data suggest that, in animal models and in humans, elevating glucocorticoid levels may reduce the development of posttraumatic stress disorder or PTSD.
This hypothesis is now supported by a new study in Biological Psychiatry. Using an animal model of PTSD, Rajnish Rao and colleagues demonstrate that elevated levels of glucocorticoids at the time of acute stress confers protection against anxiety-like behavior and the delayed enhancing effect of stress on synaptic connectivity in the basolateral amygdala.
"It seems, increasingly, that the 'trauma' in posttraumatic stress disorder is the impact of stress on brain structure and function," commented Dr. John Krystal, Editor of Biological Psychiatry. "The study by Rao and colleagues provides evidence that glucocorticoids may have protective effects in their animal model that prevent from these changes in synaptic connectivity, potentially shedding light on protective effects of glucocorticoids described in relation to PTSD."
Senior author Prof. Sumantra Chattarji from the National Centre for Biological Sciences in Bangalore, India, explained the reasoning behind their work: "First, this work was inspired by a puzzle - counterintuitive clinical reports - that individuals having lower levels of cortisol are more susceptible to developing PTSD and that cortisol treatment in turn reduces the cardinal symptoms of PTSD. Second, using a rodent model of acute stress, we were not only able to capture the essence of these clinical reports, but also identify a possible cellular mechanism in the amygdala, the emotional hub of the brain."
Their results are consistent with clinical reports on the protective effects of glucocorticoids against the development of PTSD symptoms triggered by traumatic stress.
Two successive manipulations, both of which elevate corticosterone levels by themselves, together reset the number of synapses in the amygdala and restored anxiety behavior to normal levels in rats. Strikingly, these high and low numbers of synapses in the amygdala appear to be reliable predictors of high and low anxiety states respectively.
"With the increasing costs and suffering associated with PTSD victims, it is our hope that basic research of the kind reported in this study will help in developing new therapeutic strategies against this debilitating disorder," concluded Chattarji.
The article is "Glucocorticoids Protect Against the Delayed Behavioral and Cellular Effects of Acute Stress on the Amygdala" by Rajnish P. Rao, Shobha Anilkumar, Bruce S. McEwen, and Sumantra Chattarji (doi: 10.1016/j.biopsych.2012.04.008). The article appears in Biological Psychiatry, Volume 72, Issue 6 (September 15, 2012), published by Elsevier.
Notes for editors
Full text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or Biol.Psych@utsouthwestern.edu. Journalists wishing to interview the authors may contact Sumantra Chattarji at +91 80 23666121 or firstname.lastname@example.org.
The authors' affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 5th out of 129 Psychiatry titles and 16th out of 243 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2011 Impact Factor score for Biological Psychiatry is 8.283.
Elsevier is a world-leading provider of scientific, technical and medical information products and services. The company works in partnership with the global science and health communities to publish more than 2,000 journals, including The Lancet and Cell, and close to 20,000 book titles, including major reference works from Mosby and Saunders. Elsevier's online solutions include SciVerse ScienceDirect, SciVerse Scopus, Reaxys, MD Consult and Nursing Consult, which enhance the productivity of science and health professionals, and the SciVal suite and MEDai's Pinpoint Review, which help research and health care institutions deliver better outcomes more cost-effectively.
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Media contactRhiannon Bugno
Rhiannon Bugno | EurekAlert!
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