G. Tringali et al., THE RELEASE OF IMMUNOREACTIVE INTERLEUKIN-1-BETA FROM RAT HYPOTHALAMIC EXPLANTS IS MODULATED BY NEUROTRANSMITTERS AND CORTICOTROPIN-RELEASING HORMONE, Pharmacological research, 36(4), 1997, pp. 269-273
Both constitutive and inducible interleukin-l (IL-1) gene expressions
have been described in the central nervous system, the former being as
sociated with immunoreactive IL-l neurons in human and rat hypothalami
. While most studies have focused on the role of IL-l as a mediator of
pathological events in the brain, the cytokine of neuronal origin mig
ht also be involved in the regulation of physiological processes. In t
his study we used a previously validated technique to investigate the
effects of classical neurotransmitters and the hypophysiotropic peptid
e corticotropin-releasing hormone (CRH) on the release of immunoreacti
ve (ir) IL-1 beta from acute rat hypothalamic explants. We found that
basal irIL-1 beta secretion is significantly inhibited by acetylcholin
e and histamine and increased by dopamine, while dexamethasone, IL-4 a
nd IL-10 have no effect. Moreover, cytokine release is dose-dependentl
y increased by CRH. Such effects of the neurotransmitters and CRH are
observed in short-term incubation experiments, indicating that a pre-f
ormed pool of hypothalamic IL-1 beta is involved. These findings also
suggest that the interaction between IL-1, neurotransmitters and neuro
peptides might play a role in the physiological regulation of such pro
cesses as body temperature, food intake and the control of hypothalami
c-hypophyseal axes. (C) 1997 The Italian Pharmacological Society.