title: Central nervous system IL-1 beta system and neuropeptide Y mRNAs during IL-1 beta-induced anorexia in rats.
abstract: Interleukin-1 beta (IL-1 beta) induces anorexia and neuropeptide Y (NPY) increases feeding by direct action in the central nervous system (CNS). IL-1 beta, depending on the dose, attenuates or blocks NPY-induced feeding. This suggests that IL-1 beta-NPY interactions may be involved in IL-1 beta-induced anorexia. Here, RNase protection assays were used to investigate the effects of the chronic intracerebroventricular (ICV) administration of IL-1 beta (at a dose that yields estimated pathophysiological concentrations in the cerebrospinal fluid) on mRNA levels of IL-1 beta system components and NPY in the cerebellum, parietofrontal cortex, hippocampus, hypothalamus, and midbrain. The results show that the chronic ICV administration of IL-1 beta (8.0 ng/24 h for 72 h) differentially induced IL-1 beta system components across brain regions in anorectic rats. IL-1 beta mRNA and IL-1 receptor antagonist (IL-1Ra) mRNA were induced similarly, exhibiting highest and lowest expression levels in the hypothalamus and hippocampus, respectively. IL-1 receptor type I (IL-1RI) mRNA and the soluble form of IL-1 receptor accessory protein (IL-1R AcP II) mRNA were also induced in the hypothalamus and cerebellum. NPY mRNA expression showed a small, but significant decrease in the hypothalamus. Heat-inactivated IL-1 beta (8.0 ng/24 h for 72 h) had no effect on the behavioral or molecular profiles. The results suggest that endogenous upregulation of IL-1 beta contributes to IL-1 beta-induced anorexia, and that modification of NPY mechanisms also may be involved.
authors.affiliation: Division of Molecular Biology, School of Life and Health Sciences, University of Delaware, Newark 19716-2590, USA.
authors.forename: D
authors.initials: D
authors.lastname: Gayle
authors.forename: S E
authors.initials: SE
authors.lastname: Ilyin
authors.forename: C R
authors.initials: CR
authors.lastname: Plata-Salamán
mesh_terms: D000818:Animals; D000855:Anorexia / Q000139:chemically induced* / Q000503:physiopathology*; D001835:Body Weight; D002531:Cerebellum / Q000737:chemistry / Q000502:physiology; D002540:Cerebral Cortex / Q000737:chemistry / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004326:Drinking; D004435:Eating; D015870:Gene Expression / Q000187:drug effects; D006624:Hippocampus / Q000737:chemistry / Q000502:physiology; D007031:Hypothalamus / Q000737:chemistry / Q000502:physiology; D007276:Injections, Intraventricular; D007375:Interleukin-1 / Q000235:genetics / Q000494:pharmacology*; D008297:Male; D008636:Mesencephalon / Q000737:chemistry / Q000502:physiology; D015213:Neuroimmunomodulation / Q000187:drug effects; D009478:Neuropeptide Y / Q000235:genetics*; D011506:Proteins / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018123:Receptors, Interleukin; D017472:Receptors, Interleukin-1 / Q000235:genetics; D053573:Receptors, Interleukin-1 Type I
chemical_list: C490860:Il1rl2 protein, rat; D007375:Interleukin-1; D009478:Neuropeptide Y; D011506:Proteins; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D017472:Receptors, Interleukin-1; D053573:Receptors, Interleukin-1 Type I