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Corticosteroid receptor function is decreased in depressed patients
S Modell1, A Yassouridis, J Huber
1Max Planck Institute of Psychiatry, Munich, Germany.
Neuroendocrinology
|March 1, 1997
Summary
Patients with affective disorders show impaired feedback control of the hypothalamic-pituitary-adrenocortical (HPA) system. This suggests altered glucocorticoid receptor (GR) function contributes to HPA hyperactivity in depression.
Area of Science:
- Neuroendocrinology
- Psychiatry
- Molecular Biology
Background:
- The hypothalamic-pituitary-adrenocortical (HPA) system's feedback control is often decreased in affective disorders.
- This is hypothesized to result from impaired glucocorticoid receptor (GR)-mediated feedback, failing to suppress HPA activity despite high corticosteroid levels.
Purpose of the Study:
- To investigate the dose-response relationship of the dexamethasone (DEX)/corticotropin-releasing hormone (CRH) test in depressed patients and controls.
- To test the hypothesis that altered GR capacity or function underlies exaggerated HPA activity in depression.
Main Methods:
- The DEX-CRH test was administered using three increasing doses of DEX (0.75, 1.5, 3.0 mg) to separate groups of depressed patients and healthy controls.
- Plasma adrenocorticotropin (ACTH) and cortisol levels were measured after CRH injection to assess HPA axis response.
Main Results:
- Increasing DEX doses led to decreased ACTH and cortisol release post-CRH in both groups.
- However, dose-response curves (area under the curve) for ACTH and cortisol were significantly higher in patients compared to controls, particularly at 0.75 and 1.5 mg DEX.
- The 1.5 mg DEX dose effectively differentiated between patients and controls, with differences diminishing at higher doses.
Conclusions:
- The findings support the hypothesis of altered GR capacity or function in depression.
- The DEX-CRH test, especially with a 1.5 mg DEX dose, is a valuable tool for identifying HPA axis dysregulation in affective disorders.