Naloxone-induced pituitary-adrenal activation does not differ in patients with depression, obsessive compulsive disorder, and healthy controls. Academic Article Article uri icon

Overview

MeSH

  • Adrenocorticotropic Hormone
  • Adult
  • Behavior
  • Double-Blind Method
  • Female
  • Humans
  • Hydrocortisone
  • Male
  • Stimulation, Chemical

MeSH Major

  • Depressive Disorder
  • Naloxone
  • Narcotic Antagonists
  • Obsessive-Compulsive Disorder
  • Pituitary-Adrenal System

abstract

  • Adrenocorticotropic hormone (ACTH) and cortisol secretion have been shown to be abnormal in approximately half of depressed patients. Information from pituitary and adrenal studies suggests that the locus of this dysregulation is at or above the level of the hypothalamus; however, direct evidence from provocative studies of the hypothalamic corticotropin releasing hormone (CRH) neuron does not exist. The current study was 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 subjects 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 naloxone is an effective central stimulant of the hypothalamic CRH neuron, stimulation of the hypothalamic CRH neuron with naloxone does not provide evidence of dysregulation of the HPA axis in depression.

publication date

  • August 1996

has subject area

  • Adrenocorticotropic Hormone
  • Adult
  • Behavior
  • Depressive Disorder
  • Double-Blind Method
  • Female
  • Humans
  • Hydrocortisone
  • Male
  • Naloxone
  • Narcotic Antagonists
  • Obsessive-Compulsive Disorder
  • Pituitary-Adrenal System
  • Stimulation, Chemical

Research

keywords

  • Clinical Trial
  • Comparative Study
  • Journal Article
  • Randomized Controlled Trial

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/0893-133X(95)00210-5

PubMed ID

  • 8840357

Additional Document Info

start page

  • 207

end page

  • 212

volume

  • 15

number

  • 2