PMID- 2651094
OWN - NLM
STAT- MEDLINE
DCOM- 19890606
LR  - 20181130
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 124
IP  - 5
DP  - 1989 May
TI  - In the rat, interleukin-1 alpha acts at the level of the brain and the gonads to 
      interfere with gonadotropin and sex steroid secretion.
PG  - 2105-9
AB  - These studies were designed to investigate a possible effect of the monokine 
      interleukin-1 alpha (Il-1 alpha) on gonadotropins and/or sex steroid secretion. 
      Three putative sites of action were considered: the central nervous system, the 
      pituitary, and the gonads. A central nervous system-mediated mechanism was tested 
      by injecting Il-1 alpha into the lateral ventricle of the brain of castrated 
      rats; this treatment caused a dose-related inhibition of LH secretion, with a 
      minimum effective dose below 0.1 microgram (6.6 pmol) and a maximum effect at 1 
      microgram (66 pmol). The plateau response was observed 120 min after injection. 
      The possibility that Il-1 alpha might alter pituitary sensitivity was studied by 
      administering 200 ng GnRH, iv, into gonadectomized control rats or rats 
      pretreated with 1 micrograms Il-1 alpha intracerebroventricularly. GnRH induced a 
      comparable increase in the plasma LH levels of both groups of animals. Finally, 
      hypophysectomized immature (24-day-old) female rats were used to determine if we 
      could confirm in vivo that interleukin-1 alpha can act directly at the level of 
      the ovary to interfere with steroidogenesis. In these animals, the sc injection 
      of 20 IU PMSG produced a marked (P less than 0.01) increase in plasma estradiol 
      levels, while the sequential injection of 20 IU PMSG and 1 microgram hCG 
      significantly (P less than 0.01) stimulated progesterone release. The ip 
      administration of 1 microgram Il-1 alpha every 12 h to gonadotropin-treated rats 
      resulted in a significant inhibition of both estradiol and progesterone 
      secretion. The results support possible roles for Il-1 alpha at the levels of the 
      brain and the gonads, but not the pituitary, to inhibit reproductive functions.
FAU - Rivier, C
AU  - Rivier C
AD  - Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, 
      California 92037.
FAU - Vale, W
AU  - Vale W
LA  - eng
GR  - HD-13527/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Gonadal Steroid Hormones)
RN  - 0 (Gonadotropins)
RN  - 0 (Gonadotropins, Equine)
RN  - 0 (Interleukin-1)
RN  - 0 (Pituitary Hormone-Releasing Hormones)
SB  - IM
MH  - Animals
MH  - Brain/*physiology
MH  - Drug Interactions
MH  - Female
MH  - Gonadal Steroid Hormones/*metabolism
MH  - Gonadotropins/*metabolism
MH  - Gonadotropins, Equine/pharmacology
MH  - Gonads/*physiology
MH  - Hypophysectomy
MH  - Injections, Intraventricular
MH  - Interleukin-1/pharmacology/*physiology
MH  - Male
MH  - Orchiectomy
MH  - Ovulation/drug effects
MH  - Pituitary Hormone-Releasing Hormones/physiology
MH  - Rats
MH  - Rats, Inbred Strains
EDAT- 1989/05/01 00:00
MHDA- 1989/05/01 00:01
CRDT- 1989/05/01 00:00
PHST- 1989/05/01 00:00 [pubmed]
PHST- 1989/05/01 00:01 [medline]
PHST- 1989/05/01 00:00 [entrez]
AID - 10.1210/endo-124-5-2105 [doi]
PST - ppublish
SO  - Endocrinology. 1989 May;124(5):2105-9. doi: 10.1210/endo-124-5-2105.