Abstract
Following treatment with interleukin-10 (IL-10), basal corticotrophin releasing factor (CRF) levels from rat hypothalamic median eminence (ME) were found to be increased. Our data show: (1) the specificity of stimulation of CRF through the use of recombinant IL-10 and its blockage by monoclonal anti-IL-10 antibody; (2) the requirement of NO in this process through the use of N(omega)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor; (3) the blockage of IL-10 stimulated NO production by anti-IL-10; and, (4) the presence of IL-10 transcripts in hypothalamic poly A+ mRNA. These results provide the first evidence of IL-10 acting in the ME to influence CRF levels and further support our earlier findings of a potential for IL-10 in the hypothalamic-pituitary axis.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology
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Blotting, Southern
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Corticotropin-Releasing Hormone / metabolism*
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Dose-Response Relationship, Drug
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Humans
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Interleukin-10 / genetics
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Interleukin-10 / immunology
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Interleukin-10 / pharmacology*
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Leukocytes / chemistry
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Male
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Median Eminence / drug effects
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Median Eminence / metabolism*
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NG-Nitroarginine Methyl Ester / pharmacology
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Nitric Oxide / biosynthesis*
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitric Oxide Synthase / metabolism
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Nitric Oxide Synthase Type I
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Pituitary Gland / chemistry
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RNA, Messenger / analysis
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Rats
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Rats, Wistar
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Reverse Transcriptase Polymerase Chain Reaction
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Specific Pathogen-Free Organisms
Substances
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Antibodies, Monoclonal
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RNA, Messenger
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Interleukin-10
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Nitric Oxide
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Corticotropin-Releasing Hormone
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NOS1 protein, human
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type I
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Nos1 protein, rat
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NG-Nitroarginine Methyl Ester