Updated on 10 September 2012
Say no to stress: Elevated levels of glucocorticoids at the time of acute stress, confers protection against developing post-traumatic stress disorder
Singapore: According to a new study published in Biological Psychiatry by Dr Rajnish Rao and colleagues, 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 behavior.
The article titled 'Glucocorticoids protect against the delayed behavioral and cellular effects of acute stress on the amygdala' was jointly published by Dr Rajnish P Rao, Dr Shobha Anilkumar, Dr Bruce S McEwen and Dr Sumantra Chattarji in the September issue of the magazine, which is published by Elsevier.
The new hypothesis, which was postulated by the team after using an animal model of post-traumatic stress disorder (PTSD), questions conventional views that 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.
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. For this reason, drugs such as mifepristone that block glucocorticoid activity, called glucocorticoid receptor antagonists, have been tested as treatments for depression.
Dr Sumantra Chattarji, senior author and professor, National Center for Biological Sciences (NCBS), Bangalore, India, explained the reasons behind their work. "First, this work was inspired by a puzzle, counter-intuitive 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."