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Lack of effect of interleukins 1α and 1β, during in vitro perifusion, on anterior pituitary release of adrenocorticotropic hormone and β endorphin in the male rat
Author(s) -
Parsadaniantz S. Mélik,
Lenoir V.,
Terlain B.,
Kerdelhué B.
Publication year - 1993
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490340308
Subject(s) - adrenocorticotropic hormone , medicine , endocrinology , in vivo , anterior pituitary , basal (medicine) , hormone , corticosterone , peptide hormone , pituitary gland , in vitro , interleukin , chemistry , biology , cytokine , biochemistry , microbiology and biotechnology , insulin
It has been demonstrated that interleukin 1 (IL1) injection provokes a great variety of biological effects, notably an activation of the corticotropic axis, increasing plasma adrenocorticotropic hormone (ACTH) and corticosterone. However, the primary site of action of IL1 is still controversial. In the present study, we first verified the in vivo capability of human interleukins 1α (hIL1α) and 1β (hIL1β) to release ACTH and β endorphin (β EP) in the normal male rat, before investigating, through an anterior pituitary (AP) perifusion system, the hIL1α and hIL1β effects on basal and corticotropin‐releasing factor (CRF)‐induced ACTH and β EP secretions. This system enabled the examination of a dynamic profile of hormones secretion, avoiding the possibility of feedback mechanisms, as is the case with the use of regular but very often longtime incubations. The results showed that in a perifusion system, with a short duration treatment (below 2 hr) compatible with the kinetics of action observed in vivo, basal and CRF‐induced ACTH and β EP release were not modified in the presence of a broad range of concentrations (from 10 −12 to 10 −9 M) of hIL1α or hIL1β. Taken together, these results clearly show that in an in vitro situation close to physiological conditions, the primary site of action of hIL1α and hIL1β on ACTH and β EP release is not located at the AP level in the male rat. © 1993 Wiley‐Liss, Inc.