Examples of glucocorticoid

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Stress and cortisol treatment changed affinity and number of glucocorticoid receptors in leukocytes and gill of coho salmon.
Several closed feedback mechanisms regulate the secretion of glucocorticoids.
Spontaneous and glucocorticoid-inhibited adrenocorticotropic hormone and cortisol secretion are similar in healthy young and old men.
Stress and aging may also interact to increase the vulnerability of the hippocampus to glucocorticoid mediated toxicity.
A relationship between elevated glucocorticoids and cognition has also been demonstrated in healthy subjects, suggesting the relationship is independent of disease effects.
Therefore, a relationship between glucocorticoid concentration and memory function is apparent within normal and supraphysiologic dose ranges and in states of health and disease.
There is evidence supporting a role for glucocorticoids released during stress resulting in damage to the hippocampus.
The mechanisms by which glucocorticoid-induced damage to the hippocampus takes place are not well understood.
Programming of brainstem serotonin transporter development by prenatal glucocorticoids.
They showed that glucocorticoids had modest benefit in reducing length of stay and that the benefit was partially maintained for six months.
Patients were not eligible if they had used systemic glucocorticoids up to one year prior to the study.
These findings are consistent with a relationship between high levels of glucocorticoids released during stress and hippocampal damage with associated memory deficits.
Dose-response changes in plasma cortisol and lymphocyte glucocorticoid receptors following dexamethasone administration in combat veterans with and without posttraumatic stress disorder.
The authors found that stress exposure without accompanying glucocorticoid release did not lead to stress system abnormalities normally seen among offspring exposed to prenatal stress.
Even if glucocorticoids act primarily at a peripheral level to maintain homeostasis, the brain represents one of the principal targets for these steroid hormones.
There is some evidence that glucocorticoid levels can affect cell proliferation in some parts of the central nervous system.
Postnatal handling increases hippocampal glucocorticoid receptors and enhances adrenocortical negative-feedback efficacy in the rat.
This hypercortisolism is often associated with deficient glucocorticoid receptor numbers in the lymphocytes of patients with depression.
Hippocampal apoptosis in major depression is a minor event and absent from subareas at risk for glucocorticoid overexposure.

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