NALOXONE-INDUCED PITUITARY-ADRENAL ACTIVATION DOES NOT DIFFER IN PATIENTS WITH DEPRESSION, OBSESSIVE-COMPULSIVE DISORDER, AND HEALTHY CONTROLS

Adrenocorticotropic hormone (ACTH) and cortisol secretion have been sh own to be abnormal in approximately half of depressed patients. Inform ation from pituitary and adrenal studies suggests that the focus of th is dysregulation is at or above the level of the hypothalamus; however ; direct evidence from provocative studies of the hypothalamic cortico tropin releasing hormone (CRH) neuron does Mot exist. The current stud y teas designed to stimulate hypothalamic CRH release using the opiate antagonist naloxone in patients with depression and elevated urinary- free cortisols as well as healthy and psychiatric controls. All subjec ts received naloxone and placebo on separate days in a double-blinded, randomized fashion at a dose determined previously to reliably induce significant increases in ACTH and cortisol secretion. No significant differences were noted among groups. We conclude that although naloxon e is an effective central stimulant of the hypothalamic CRH neuron, st imulation of the hypothalamic CRH neuron with naloxone does not provid e evidence of dysregulation of the HPA axis in depression.