PMID- 9152627
OWN - NLM
STAT- MEDLINE
DCOM- 19970820
LR  - 20190905
IS  - 0918-8959 (Print)
IS  - 0918-8959 (Linking)
VI  - 44
IP  - 1
DP  - 1997 Feb
TI  - Tumor necrosis factor-alpha mediates endotoxin induced suppression of 
      gonadotropin-releasing hormone pulse generator activity in the rat.
PG  - 141-8
AB  - Bacterial endotoxin lipopolysaccharide (LPS) is known to suppress gonadotropin 
      secretion and this effect is assumed to be mediated by cytokines. In the present 
      study, we examined whether LPS affected hypothalamic electrical activity 
      associated with LH pulses, and whether tumor necrosis factor-alpha (TNF-alpha), a 
      major cytokine induced by LPS, was involved in this process. Ovariectomized rats 
      were fitted with chronically implanted electrode arrays in the mediobasal 
      hypothalamus, and multiunit activity (MUA) was recorded under conscious, 
      unrestrained conditions. Blood samples were withdrawn every 6 min through an 
      indwelling atrial catheter or determining serum LH concentrations. Intravenous 
      (i.v.) injection of LPS (1 microgram) suppressed characteristic increases 
      (volleys) in MUA associated with LH pulses throughout the experimental period up 
      to 5 h. This suppressive effect of LPS on MUA volleys was significantly 
      attenuated by simultaneous intracerebroventricular (icv) injection of the 
      antibody (50 ng) to TNF-alpha through an indwelling cannula in the lateral 
      ventricle. These changes in MUA were faithfully reflected in the LH secretory 
      pattern. Further, either i.v. (0.4-2 micrograms) or i.c.v. (20-250 ng) injection 
      of TNF-alpha suppressed the frequency of MUA volleys and associated LH pulses in 
      a dose-dependent manner. These results suggest that LPS leads to the suppression 
      of gonadotropin-releasing hormone pulse generator activity through a mechanism 
      involving TNF-alpha.
FAU - Yoo, M J
AU  - Yoo MJ
AD  - Department of Veterinary Physiology, Veterinary Medical Science, University of 
      Tokyo, Japan.
FAU - Nishihara, M
AU  - Nishihara M
FAU - Takahashi, M
AU  - Takahashi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Endocr J
JT  - Endocrine journal
JID - 9313485
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 9002-67-9 (Luteinizing Hormone)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/administration & dosage/immunology
MH  - Dose-Response Relationship, Drug
MH  - Electrodes, Implanted
MH  - Electrophysiology
MH  - Female
MH  - Gonadotropin-Releasing Hormone/*physiology
MH  - Hypothalamus, Middle/drug effects/*physiology
MH  - Injections, Intravenous
MH  - Injections, Intraventricular
MH  - Lipopolysaccharides/administration & dosage/*pharmacology
MH  - Luteinizing Hormone/*blood/drug effects
MH  - Mice
MH  - Rats
MH  - Rats, Wistar
MH  - Recombinant Proteins/administration & dosage
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/administration & dosage/immunology/*physiology
EDAT- 1997/02/01 00:00
MHDA- 1997/02/01 00:01
CRDT- 1997/02/01 00:00
PHST- 1997/02/01 00:00 [pubmed]
PHST- 1997/02/01 00:01 [medline]
PHST- 1997/02/01 00:00 [entrez]
AID - 10.1507/endocrj.44.141 [doi]
PST - ppublish
SO  - Endocr J. 1997 Feb;44(1):141-8. doi: 10.1507/endocrj.44.141.