Researchers at the National Centre for Biological Sciences (NCBS), Bengaluru have found that the presence of glucocorticoids, a group of stress hormones, are shown to be beneficial to reduce the development of post traumatic stress disorder (PTSD).

The research has indicated that in animal models and in humans, elevating glucocorticoid levels are proving to be advantageous because it helps the body and mind to cope with stress during post trauma.

The study was supported by a Wellcome Trust Senior Research Fellowship to Prof. Sumantra Chattarji from the NCBS; International Brain Research Organization and Sarojini Damodaran International Fellowships to Rajnish P Rao; and Lightfighter Trust and National Institute of Mental Health Grant No. 5P50MH58911 to Joseph LeDoux, principal investigator, Biomedical Engineering at the Georgia Tech and Emory University.

Using an animal model of PTSD, Rajnish Rao and colleagues including Prof. Chattarji and Shobha Anilkumar demonstrated that elevated levels of glucocorticoids at the time of acute stress confers protection against the delayed enhancing effect of stress on synaptic connectivity in the basolateral amygdala and anxiety-like behaviour.

According to the researchers, for this reason, drugs such as mifepristone that block glucocorticoid activity, called glucocorticoid receptor antagonists, have been tested as treatments for depression.

Glucocorticoids 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.

“First, this work was inspired by a puzzle or a counterintuitive clinical report 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,” said Prof. Chattarji.

Now the results are consistent with clinical reports on the protective effects of glucocorticoids against the development of PTSD symptoms triggered by traumatic stress, added Prof. Chattarji.

Two successive manipulations, both of which elevate corticosterone levels by themselves, together reset the number of synapses in the amygdala and restored anxiety behaviour 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, said Prof. Chattarji.

“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,” stated Chattarji.