Abstract
Central mechanisms for the attenuating effects of fetal alcohol exposure (FAE) on interleukin-1beta (IL-1beta)-induced fever were studied in adult male offspring of dams fed a liquid diet supplemented with ethanol (E), in pair-fed (P) control and in normal (N) offspring. Hypothalamic levels of IL-1 were significantly lower in E than in N rats at 2 h, but not at 4 and 6 h, after intraperitoneal administration of lipopolysaccharide. Fever induced by intracerebroventricular (i.c.v.) IL-1 was significantly lower in E than in N and P rats. In contrast, E rats showed a normal febrile response to i.c.v. prostaglandin-E2. Thus, whereas FAE does not affect central thermoregulatory mechanisms, per se, FAE alters the kinetics of hypothalamic IL-1 production/appearance and decreases the responsiveness of central mechanisms which mediate the febrile response to IL-1.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adrenocorticotropic Hormone / blood
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Alcoholism / physiopathology
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Animals
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Body Temperature Regulation / drug effects*
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Corticosterone / blood
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Dinoprostone / toxicity
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Drinking / drug effects
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Eating / drug effects
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Ethanol / toxicity
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Female
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Fetal Alcohol Spectrum Disorders / immunology*
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Fever / chemically induced
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Fever / prevention & control*
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Hypothalamus / chemistry
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Immunologic Deficiency Syndromes / chemically induced*
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Injections, Intraventricular
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Interleukin-1 / administration & dosage
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Interleukin-1 / analysis
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Interleukin-1 / toxicity*
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Interleukin-10 / analysis
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Interleukin-6 / analysis
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Lipopolysaccharides / toxicity
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Locomotion / drug effects
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Male
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Neuroimmunomodulation*
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Pregnancy
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Pregnancy Complications
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Prenatal Exposure Delayed Effects
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Rats
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Rats, Sprague-Dawley
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Tumor Necrosis Factor-alpha / analysis
Substances
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Interleukin-1
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Interleukin-6
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Lipopolysaccharides
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Tumor Necrosis Factor-alpha
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Interleukin-10
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Ethanol
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Adrenocorticotropic Hormone
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Dinoprostone
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Corticosterone