Noradrenaline release in hypothalamus and ACTH secretion induced by central interleukin-1beta.
The effect of interleukin-1beta (IL-1beta, 10 ng per 5 mu l i.c.v.) on noradrenaline release in the hypothalamus of freely moving rats and on plasma ACTH levels has been studied, respectively by intracerebral microdialysis and radioimmunoassay. IL-1beta induced an early increase in noradrenaline (NA) release in the paraventricular nucleus (PVN) followed by a second long-lasting enhancement starting from 80 min, with a maximum at 140 min (187 +/- 14%). Heat-denatured IL-1beta induced only the early increase without any other change at later times. IL-1beta did not significantly affect NA release in the area surrounding the PVN at any time. IL-1beta increased ACTH levels at 2 and 3 h. Indomethacin (10 mg kg(-1), i.p.) prevented the noradrenergic and ACTH responses. The NA system in the PVN plays a part in the mechanism controlling the ACTH response induced by IL-1.
Terrazzino
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S
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
Perego
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C
De Simoni
M G
MG
D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D007031:Hypothalamus / Q000187:drug effects*; D007213:Indomethacin / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D007375:Interleukin-1; D000324:Adrenocorticotropic Hormone; D009638:Norepinephrine; D007213:Indomethacin