INTERLEUKIN-1 STIMULATES ACTH RELEASE BY AN INDIRECT ACTION WHICH REQUIRES ENDOGENOUS CORTICOTROPIN RELEASING FACTOR

作者：Akira Uehara, Paul E. Gottschall, Raymond R. Dahl, Akira Arimura · 发表于：Endocrinology · 年份：1987 · DOI：10.1210/endo-121-4-1580 · 被引用次数：340 · 研究领域：Stress Responses and Cortisol、Adrenal Hormones and Disorders、Tryptophan and brain disorders

The present study was performed in order to clarify the mechanism by which interleukin-1 (IL-1) activates the hypothalamic-pituitary-adrenal (H-P-A) axis. The iv administration of IL-1 into freely moving, conscious rats significantly elevated the plasma levels of ACTH. This ACTH response to IL-1 was, however, completely abolished by preinjection of 0.5 ml rabbit antiserum generated against rat CRF, but not by normal rabbit serum (NRS). The IL-1-induced ACTH release did not seem to be caused by a general stress effect of IL-1 because plasma PRL levels, another indicator of a stress response, were not altered by the injection of IL-1. These results suggest that IL-1 acts centrally in the brain to stimulate the secretion of CRF, thereby eliciting ACTH release, and that a direct action of IL-1 on the pituitary gland is unlikely.