Increased biogenic amine release in mouse hypothalamus following immunological challenge: antagonism by indomethacin.
Stimulation of the acute-phase response in mice by lipopolysaccharide, pokeweed mitogen, concanavalin A or interleukin-1 was associated with increased release of biogenic amines, serotonin and norepinephrine in the hypothalamus as indexed by their primary metabolites, 5-hydroxyindoleacetic acid and 3-methoxy-4-hydroxyphenylglycol, respectively. The increases in norepinephrine and serotonin turnover observed 4 h following systemic administration of interleukin-1 were antagonized by concurrent administration of indomethacin, a potent inhibitor of cyclooxygenase. These data suggest that the increase in norepinephrine and serotonin release in mouse hypothalamus during the acute-phase response to infection is partially mediated by the actions of arachidonic acid metabolites.
Mefford
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Section on Clinical Pharmacology, Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892.
Heyes
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MP
D000818:Animals; D001679:Biogenic Amines / Q000037:antagonists & inhibitors / Q000378:metabolism*; D003208:Concanavalin A / Q000494:pharmacology; D007031:Hypothalamus / Q000378:metabolism*; D007107:Immune System / Q000502:physiology*; D007213:Indomethacin / Q000494:pharmacology*; D007375:Interleukin-1 / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011043:Pokeweed Mitogens / Q000494:pharmacology
D001679:Biogenic Amines; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011043:Pokeweed Mitogens; D003208:Concanavalin A; D007213:Indomethacin