Apr 4, 2001

Central monoamine and plasma corticosterone changes induced by a bacterial endotoxin: sensitization and cross-sensitization effects

The European Journal of Neuroscience
Shawn HayleyHymie Anisman

Abstract

Low doses of lipopolysaccharide, tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), or exposure to a stressor (restraint) increased plasma corticosterone levels. In animals pretreated with lipopolysaccharide, a marked sensitization of the corticosterone response was evident upon subsequent exposure to lipopolysaccharide, TNF-alpha, or restraint, 1 day later. As well, the sickness-inducing effects of lipopolysaccharide, TNF-alpha and IL-1 beta were markedly increased in mice pretreated with lipopolysaccharide. The sensitization effects were marked when the second treatment was administered 1 day after lipopolysaccharide administration, but not when a 28-day interval elapsed. In a second experiment, TNF-alpha influenced monoamine functioning in the paraventricular nucleus of the hypothalamus and within extrahypothalamic regions, including the central amygdala, locus coeruleus, prefrontal cortex. Moreover, serotonin activity within the central amygdala, as well as dopamine activity within the prefrontal cortex, were subject to a sensitization effect in animals pretreated with lipopolysaccharide 1 day earlier. Macrophage depletion by a suspension of clodronate liposomes attenuated the plasma corticosterone ch...Continue Reading

Mentioned in this Paper

Behavior, Animal
Variolation
Tumor Necrosis Factor-alpha
Tnf
Brain
Tumor Lysis Syndrome
Cross Reactions
Lipopolysaccharides
Biogenic Monoamines
Central Cord Syndrome

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