Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors

Robert J Handa, Karin M. Nunley, Stanley A. Lorens, Jeffrey P. Louie, Robert F. McGivern, Melanie R. Bollnow

Research output: Contribution to journalArticle

255 Citations (Scopus)

Abstract

To examine mechanisms responsible for sex differences in hypothalamo-pituitary-adrenal (HPA) axis responsiveness to stress, we studied the role of androgens in the regulation of the adrenocorticotropin (ACTH) and corticosterone (CORT) responses to foot shock and novelty stressors in gonadectomized (GDX) or intact male F344 rats. Foot shock or exposure to a novel open field increased plasma ACTH and CORT, which was significantly greater in GDX vs. intacts. Testosterone (T) or dihydrotestosterone propionate (DHT) treatment of GDX animals returned poststress levels of ACTH and CORT to intact levels. Estrogen treatment of GDX males further increased poststress CORT secretion above GDX levels. There was no difference in the ACTH response of anterior pituitaries from intact, GDX, and GDX + DHT animals to CRF using an in vitro perifusion system. There were no differences in βmax or binding affinity of type I or II CORT receptors in the hypothalamus or hippocampus of intact, GDX, or GDX + DHT groups. These data demonstrate an effect of GDX on hormonal indices of stress. The increased response in GDX rats appears to be due to the release from androgen receptor mediated inhibition of the HPA axis. This inhibition by androgen is not due to changes in anterior pituitary sensitivity to CRH, nor to changes in type I or type II corticosteroid receptor concentrations.

Original languageEnglish (US)
Pages (from-to)117-124
Number of pages8
JournalPhysiology and Behavior
Volume55
Issue number1
DOIs
StatePublished - 1994
Externally publishedYes

Fingerprint

Corticosterone
Adrenocorticotropic Hormone
Androgens
Foot
Shock
Safe Sex
Testosterone Propionate
Steroid Receptors
Inbred F344 Rats
Androgen Receptors
Sex Characteristics
Hypothalamus
Hippocampus
Estrogens
dihydrotestosterone propionate
Inhibition (Psychology)

Keywords

  • ACTH
  • Androgen
  • Corticosterone
  • CRH
  • Dihydrotestosterone
  • Estrogen
  • Glucocorticoid receptor
  • Mineralocorticoid receptor
  • Testosterone

ASJC Scopus subject areas

  • Physiology (medical)
  • Behavioral Neuroscience

Cite this

Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors. / Handa, Robert J; Nunley, Karin M.; Lorens, Stanley A.; Louie, Jeffrey P.; McGivern, Robert F.; Bollnow, Melanie R.

In: Physiology and Behavior, Vol. 55, No. 1, 1994, p. 117-124.

Research output: Contribution to journalArticle

Handa, Robert J ; Nunley, Karin M. ; Lorens, Stanley A. ; Louie, Jeffrey P. ; McGivern, Robert F. ; Bollnow, Melanie R. / Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors. In: Physiology and Behavior. 1994 ; Vol. 55, No. 1. pp. 117-124.
@article{1bcea8aa53dd4fdf88743cd6cf45a42c,
title = "Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors",
abstract = "To examine mechanisms responsible for sex differences in hypothalamo-pituitary-adrenal (HPA) axis responsiveness to stress, we studied the role of androgens in the regulation of the adrenocorticotropin (ACTH) and corticosterone (CORT) responses to foot shock and novelty stressors in gonadectomized (GDX) or intact male F344 rats. Foot shock or exposure to a novel open field increased plasma ACTH and CORT, which was significantly greater in GDX vs. intacts. Testosterone (T) or dihydrotestosterone propionate (DHT) treatment of GDX animals returned poststress levels of ACTH and CORT to intact levels. Estrogen treatment of GDX males further increased poststress CORT secretion above GDX levels. There was no difference in the ACTH response of anterior pituitaries from intact, GDX, and GDX + DHT animals to CRF using an in vitro perifusion system. There were no differences in βmax or binding affinity of type I or II CORT receptors in the hypothalamus or hippocampus of intact, GDX, or GDX + DHT groups. These data demonstrate an effect of GDX on hormonal indices of stress. The increased response in GDX rats appears to be due to the release from androgen receptor mediated inhibition of the HPA axis. This inhibition by androgen is not due to changes in anterior pituitary sensitivity to CRH, nor to changes in type I or type II corticosteroid receptor concentrations.",
keywords = "ACTH, Androgen, Corticosterone, CRH, Dihydrotestosterone, Estrogen, Glucocorticoid receptor, Mineralocorticoid receptor, Testosterone",
author = "Handa, {Robert J} and Nunley, {Karin M.} and Lorens, {Stanley A.} and Louie, {Jeffrey P.} and McGivern, {Robert F.} and Bollnow, {Melanie R.}",
year = "1994",
doi = "10.1016/0031-9384(94)90018-3",
language = "English (US)",
volume = "55",
pages = "117--124",
journal = "Physiology and Behavior",
issn = "0031-9384",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors

AU - Handa, Robert J

AU - Nunley, Karin M.

AU - Lorens, Stanley A.

AU - Louie, Jeffrey P.

AU - McGivern, Robert F.

AU - Bollnow, Melanie R.

PY - 1994

Y1 - 1994

N2 - To examine mechanisms responsible for sex differences in hypothalamo-pituitary-adrenal (HPA) axis responsiveness to stress, we studied the role of androgens in the regulation of the adrenocorticotropin (ACTH) and corticosterone (CORT) responses to foot shock and novelty stressors in gonadectomized (GDX) or intact male F344 rats. Foot shock or exposure to a novel open field increased plasma ACTH and CORT, which was significantly greater in GDX vs. intacts. Testosterone (T) or dihydrotestosterone propionate (DHT) treatment of GDX animals returned poststress levels of ACTH and CORT to intact levels. Estrogen treatment of GDX males further increased poststress CORT secretion above GDX levels. There was no difference in the ACTH response of anterior pituitaries from intact, GDX, and GDX + DHT animals to CRF using an in vitro perifusion system. There were no differences in βmax or binding affinity of type I or II CORT receptors in the hypothalamus or hippocampus of intact, GDX, or GDX + DHT groups. These data demonstrate an effect of GDX on hormonal indices of stress. The increased response in GDX rats appears to be due to the release from androgen receptor mediated inhibition of the HPA axis. This inhibition by androgen is not due to changes in anterior pituitary sensitivity to CRH, nor to changes in type I or type II corticosteroid receptor concentrations.

AB - To examine mechanisms responsible for sex differences in hypothalamo-pituitary-adrenal (HPA) axis responsiveness to stress, we studied the role of androgens in the regulation of the adrenocorticotropin (ACTH) and corticosterone (CORT) responses to foot shock and novelty stressors in gonadectomized (GDX) or intact male F344 rats. Foot shock or exposure to a novel open field increased plasma ACTH and CORT, which was significantly greater in GDX vs. intacts. Testosterone (T) or dihydrotestosterone propionate (DHT) treatment of GDX animals returned poststress levels of ACTH and CORT to intact levels. Estrogen treatment of GDX males further increased poststress CORT secretion above GDX levels. There was no difference in the ACTH response of anterior pituitaries from intact, GDX, and GDX + DHT animals to CRF using an in vitro perifusion system. There were no differences in βmax or binding affinity of type I or II CORT receptors in the hypothalamus or hippocampus of intact, GDX, or GDX + DHT groups. These data demonstrate an effect of GDX on hormonal indices of stress. The increased response in GDX rats appears to be due to the release from androgen receptor mediated inhibition of the HPA axis. This inhibition by androgen is not due to changes in anterior pituitary sensitivity to CRH, nor to changes in type I or type II corticosteroid receptor concentrations.

KW - ACTH

KW - Androgen

KW - Corticosterone

KW - CRH

KW - Dihydrotestosterone

KW - Estrogen

KW - Glucocorticoid receptor

KW - Mineralocorticoid receptor

KW - Testosterone

UR - http://www.scopus.com/inward/record.url?scp=0028366293&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028366293&partnerID=8YFLogxK

U2 - 10.1016/0031-9384(94)90018-3

DO - 10.1016/0031-9384(94)90018-3

M3 - Article

C2 - 8140154

AN - SCOPUS:0028366293

VL - 55

SP - 117

EP - 124

JO - Physiology and Behavior

JF - Physiology and Behavior

SN - 0031-9384

IS - 1

ER -