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Journal of Neuroscience, Vol 15, 1961-1970, Copyright © 1995 by Society for Neuroscience
Involvement of interleukin-1 in immobilization stress-induced increase in plasma adrenocorticotropic hormone and in release of hypothalamic monoamines in the rat
F Shintani, T Nakaki, S Kanba, K Sato, G Yagi, M Shiozawa, S Aiso, R Kato and M Asai
Department of Neuro-psychiatry, Keio University School of Medicine, Tokyo, Japan.
We investigated whether interleukin-1 (IL-1) activity in the rat
hypothalamus was increased by immobilization stress (IS), and whether
pretreatment with an interleukin-1 receptor antagonist (IL-1Ra) is capable
of inhibiting IS-induced elevations of hypothalamic norepinephrine (NE),
dopamine (DA), and serotonin (5-HT) and the levels of their metabolites as
well as of plasma adrenocorticotropic hormone (ACTH). IL-1 activity was
estimated with a bioassay using mouse thymocyte proliferation in the
presence of concanavalin A. IL-1Ra was administered directly into the
anterior hypothalamus, and monoamines were determined using a microdialysis
technique and an HPLC system. First, we found that levels of IL-1 activity
in the rat hypothalamus reached a maximum at 60 min after starting IS.
Second, IL-1Ra (2 micrograms) significantly inhibited IS-induced increases
in hypothalamic NE, DA, and 5-HT levels as well as the levels of their
metabolites. In addition, IL-1Ra (2 micrograms) also inhibited the IS-
induced elevation of plasma ACTH levels. Third, timing effects of IL- 1Ra
administration on the IS-induced monoamines or ACTH responses were
examined. IL-1Ra (2 micrograms) administered at 5 or 60 min before the
start of IS, but not at 5 or 60 min after IS had been started, exerted
inhibitory effects on these responses, indicating that the effects of IL-1
occurred within 5 min after the initiation of IS. In summary, these results
suggest that IS enhances biologically active IL-1 in the hypothalamus, and
that hypothalamic IL-1 plays a role in the regulation of IS-induced
responses including elevated monoamine release in the hypothalamus and
activation of the hypothalamo-pituitary-adrenal axis. Moreover, since 5 min
is too short a time for IS to induce production of IL-1, IS may augment the
effects of preexisting IL-1 in the hypothalamus.
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