Abstract

Sickness behavior refers to a coordinated set of behavioral changes that develop in sick individuals during the course of an infection. These changes are due to the effects of proinflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α) on brain cellular targets and represent the expression of a well organized central motivational state. Based on the results of pharmacological and biochemical experiments, it is now apparent that sickness behavior is mediated by cytokines which are temporarily expressed in the brain in response to peripheral cytokines. Centrally released cytokines act on brain receptors which are identical to those characterized on immune cells. Primary afferent nerves represent the main communication pathway between peripheral and central cytokines. The sickness inducing effects of cytokines are downregulated by a number of endogenous neuropeptides and hormones, including vasopressin and glucocorticoids.KeywordsBehavioral EffectChronic Fatigue SyndromeCorticotrophin Release FactorConditioned Taste AversionCytokine ActionThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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