Systemic administration of the proinflammatory cytokine, tumor necrosis factor-α (TNF-α), has acute as well as sensitizing effects on behavioral and neurochemical functioning. Objectives: As many of the central consequences of TNF-α are mediated by its p55 receptor, the present investigation determined the role of this receptor on the plasma corticosterone increase associated with the acute TNF-α treatment and the sensitized response evident upon reexposure to the cytokine. Moreover, the role of p55 in the provocation of corticosterone release engendered by lipopolysaccharide (LPS) and psychogenic stressors (noise or restraint) was also determined. Methods: Plasma corticosterone levels were determined in wild-type and p55-deficient mice that received systemic treatments with TNF-α and LPS, as well as exposure to auditory and restraint stressors. Results: Mice deficient for p55 displayed a greatly attenuated plasma corticosterone response to TNF-α irrespective of whether they had been previously exposed to the cytokine. In contrast, p55 deletion did not affect corticosterone responses elicited by LPS and by stressors. Conclusions: It appears that although p55 modulates the corticosterone-inducing effects of TNF-α, the receptor does not play a critical role in the activation of the HPA axis by ‘traditional’ psychogenic stressors (noise, restraint) or systemic endotoxin challenge.

Keywords:
Tumor necrosis factor-α, Corticosterone, Sensitization, Knockout
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© 2004 S. Karger AG, Basel
2004
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