You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


Advertisement

ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | RSS | Access Rights | Sign In


  Vol. 47 No. 5, May 1990 TABLE OF CONTENTS
  Online Only
 •  Online First Table of
Contents
  ORIGINAL ARTICLES
 •Online Features
 This Article
 •References
 •Full text PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (43)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Delicious Add to Digg Add to Facebook Add to Reddit Add to Technorati Add to Twitter What's this?

β-Lipotropin—β-Endorphin Response to Low-Dose Ovine Corticotropin Releasing Factor in Endogenous Depression

Preliminary Studies

Elizabeth A. Young, MD; Stanley J. Watson, MD, PhD; Joan Kotun, MD; Roger F. Haskett, MD; Leon Grunhaus, MD; Virginia Murphy-Weinberg, RN; Wylie Vale, PhD; Jean Rivier, PhD; Huda Akil, PhD

Arch Gen Psychiatry. 1990;47(5):449-457.


Abstract



• Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, β-lipotropin—β-endorphin. We observed a decreased β-lipotropin—β-endorphin response in depressed subjects, but a normal adrenal cortisol response. Although the total β-lirotropin—β-endorphin response was decreased, the initial secretory response did not differ between patients and normal controls. Rather, the patients appeared to turn off secretion faster. This rapid shutoff was seen in all patients regardless of resting cortisol levels, suggesting that resting cortisol levels alone do not explain the decreased response seen in depressed patients.



Author Affiliations



From the Mental Health Research Institute, Department of Psychiatry, University of Michigan, Ann Arbor (Drs Young, Watson, Kotun, Haskett, Grunhaus, and Akil and Ms Murphy-Weinberg); and the Clayton Foundation, Laboratories for Peptide Biology, the Salk Institute, La Jolla, Calif (Drs Vale and Rivier).


Footnotes



Accepted for publication August 16, 1989.

Read in part before the 41st Annual Society of Biological Psychiatry Meeting, Washington, DC, May 9, 1986.

Reprint requests to Mental Health Research Institute, University of Michigan, 205 Washtenaw Pl, Ann Arbor, MI 48109-0720 (Dr Young).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Delicious Delicious   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Depression in Patients With Cancer: Diagnosis, Biology, and Treatment
McDaniel et al.
Arch Gen Psychiatry 1995;52:89-99.
ABSTRACT  

Loss of Glucocorticoid Fast Feedback in Depression
Young et al.
Arch Gen Psychiatry 1991;48:693-699.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | PHYSICIAN JOBS | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1990 American Medical Association. All Rights Reserved.