PMID- 8392427
OWN - NLM
STAT- MEDLINE
DCOM- 19930813
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 612
IP  - 1-2
DP  - 1993 May 28
TI  - Mode of action of interleukin-1 in suppression of pituitary LH release in 
      castrated male rats.
PG  - 1-8
AB  - These studies were undertaken to elucidate the mechanisms whereby the cytokine, 
      Interleukin (IL-1) suppresses pituitary LH release in orchidectomized rats. Since 
      LH secretion is pulsatile in castrated rats, the effects of IL-1 on the 
      components of the LH pulsatility were assessed. Intracerebroventricular (i.c.v.) 
      administration of IL-1 alpha or IL-1 beta suppressed LH release, but IL-1 beta 
      was relatively more effective than IL-1 alpha in terms of the onset (IL-1 beta = 
      30 min; IL-1 alpha = 105 min) as well as the magnitude and duration of LH 
      suppression. Further, the marked suppression of LH secretion in IL-1 beta-treated 
      rats was found to be due to significant reductions both in the frequency and 
      amplitude of LH episodes. We next evaluated whether the IL-1 beta-induced 
      suppression of LH release was mediated by either of the two inhibitory 
      hypothalamic peptidergic systems, corticotrophin releasing hormone (CRH) and 
      endogenous opioid peptides (EOP). Passive immunoneutralization of CRH by i.c.v. 
      administration of a specific CRH-antibody, either once at 15 min or twice at 75 
      and 15 min before IL-1 beta injection, failed to block the suppressive effects of 
      IL-1 beta on LH release. Similarly, pharmacological blockade of CRH by i.c.v. 
      injection of the CRH receptor antagonist, alpha-helical CRH9-41 15 min before 
      IL-1 beta was ineffective. However, i.v. infusion of the opiate receptor 
      antagonist, naloxone, which on its own had no effect on LH secretion, 
      counteracted the inhibitory effects of IL-1 beta. To further identify the opiate 
      receptor subtype involved, we utilized specific opiate receptor subtype 
      antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Bonavera, J J
AU  - Bonavera JJ
AD  - Department of Obstetrics and Gynecology, University of Florida College of 
      Medicine, Gainesville 32610.
FAU - Kalra, S P
AU  - Kalra SP
FAU - Kalra, P S
AU  - Kalra PS
LA  - eng
GR  - HD11362/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Interleukin-1)
RN  - 0 (Narcotic Antagonists)
RN  - 0 (Receptors, Opioid)
RN  - 36B82AMQ7N (Naloxone)
RN  - 36OOQ86QM1 (norbinaltorphimine)
RN  - 5S6W795CQM (Naltrexone)
RN  - 72782-05-9 (beta-funaltrexamine)
RN  - 9002-67-9 (Luteinizing Hormone)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
SB  - IM
MH  - Animals
MH  - Corticotropin-Releasing Hormone/antagonists & inhibitors/immunology/metabolism
MH  - Depression, Chemical
MH  - Hypothalamus/physiology
MH  - Injections, Intraventricular
MH  - Interleukin-1/*pharmacology
MH  - Luteinizing Hormone/*metabolism
MH  - Male
MH  - Naloxone/pharmacology
MH  - Naltrexone/analogs & derivatives/pharmacology
MH  - Narcotic Antagonists/pharmacology
MH  - Orchiectomy
MH  - Pituitary Gland/drug effects/*metabolism
MH  - Rats
MH  - Receptors, Opioid/drug effects
EDAT- 1993/05/28 00:00
MHDA- 1993/05/28 00:01
CRDT- 1993/05/28 00:00
PHST- 1993/05/28 00:00 [pubmed]
PHST- 1993/05/28 00:01 [medline]
PHST- 1993/05/28 00:00 [entrez]
AID - 0006-8993(93)91637-8 [pii]
AID - 10.1016/0006-8993(93)91637-8 [doi]
PST - ppublish
SO  - Brain Res. 1993 May 28;612(1-2):1-8. doi: 10.1016/0006-8993(93)91637-8.