Murine tumor necrosis factor-α (mTNF-α) results in the sensitization of mechanisms underlying plasma corticosterone activity and sickness behavior, the latter being reminiscent of septic or anaphylactic shock. The mTNF-α induced a sensitization of sickness and corticosterone in mice that was attenuated by pretreatment with the combinations of histamine H1 (diphenhydramine, mepyramine) and H2 (cimetidine) antagonists. Likewise, coadministration of diphenhydramine and cimetidine prevented the mTNF-α-provoked rise of monoamine activity within the posterior hypothalamus. Although dexamethasone ameliorated the mTNF-α-induced sensitization of corticosterone, illness behavior was unaffected. It is suggested that mTNF-α-induced illness and the neuroendocrine sensitization are mediated by endogenous histamine.

Additional Metadata
Keywords Corticosterone, Histamine, Sensitization, Shock, Sickness, TNF-α
Persistent URL dx.doi.org/10.1016/S0165-5728(02)00259-X
Journal Journal of Neuroimmunology
Citation
Hayley, S, Kelly, O., & Anisman, H. (2002). Murine tumor necrosis factor-α sensitizes plasma corticosterone activity and the manifestation of shock: Modulation by histamine. Journal of Neuroimmunology, 131(1-2), 60–69. doi:10.1016/S0165-5728(02)00259-X