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 ω -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.
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