Abstract
A substantial body of data suggests that excessive cortisol secretion in depression may result from a dysregulation at several sites within the hypothalamic-pituitary-adrenocortical (HPA) axis. These alterations in regulatory mechanisms are thought to be the result of a hypothalamic 'overdrive' of corticotropin-releasing hormone (CRH). Previous studies have demonstrated a diminished adrenocorticotropin (ACTH) secretory response, as well as a heightened adrenocortical responsiveness after ovine-CRH administration in depressed patients. In the present investigation, we examined pituitary and adrenocortical responsiveness after an ovine-CRH stimulation test before and during clinical recovery in seven depressed patients. Cumulative ACTH responses increased significantly during clinical recovery (P=0.014). Paradoxically, maximum and peak cortisol responses increased after recovery, suggesting that heightened adrenocortical responsiveness to ACTH during depression may take longer to 'normalize' than abnormal pituitary responsiveness to ovine-CRH stimulation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 213-222 |
| Number of pages | 10 |
| Journal | Journal of Affective Disorders |
| Volume | 14 |
| Issue number | 3 |
| DOIs | |
| State | Published - 1988 |
| Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Clinical Psychology
- Psychiatry and Mental health