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Inhibition by neuropeptides of interleukin‐1β‐induced, prostaglandin‐independent hyperalgesia
Author(s) -
Follenfant R.L.,
NakamuraCraig M.,
Henderson B.,
Higgs G.A.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb16860.x
Subject(s) - hyperalgesia , neuropeptide , endocrinology , prostaglandin , prostaglandin e2 , medicine , chemistry , beta (programming language) , stimulation , alpha (finance) , prostaglandin e , pharmacology , nociception , receptor , construct validity , nursing , computer science , patient satisfaction , programming language
The cytokine interleukin‐1β (IL‐lβ) is a potent hyperalgesic agent in the rat whereas IL‐1α is relatively inactive (Ferreira et al. , 1988). IL‐1β induced a dose‐dependent increase in the sensitivity of rat paws to mechanical stimulation following intra‐plantar injection but this effect was not reduced by indomethacin (1.0 mg kg −1 , p.o.), at a dose known to inhibit completely prostaglandin synthesis in the rat (Salmon et al. , 1983). Prostaglandin (PG)E 2 enhanced sensitivity to both mechanical pressure and increased temperature but IL‐1β enhanced only sensitivity to pressure. These observations indicate that IL‐1β sensitized pressure‐sensitive but not temperature‐sensitive sensory neurones, through a prostaglandin‐independent mechanism. Hyperalgesia induced by IL‐1β but not PGE 2 , was inhibited by the neuropeptide melanocyte‐stimulating hormone (αMSH) and its analogue [Nle 4 , D‐Phe 7 ] αMSH which are known to antagonize IL‐1 responses in other systems (Holdeman & Lipton, 1985; Cannon et al. , 1986). IL‐1β induced hyperalgesia was also reduced by the putative IL‐1β antagonist Lys‐D‐Pro‐Thr (Ferreira et al. , 1988) but αMSH and its analogue were 10–50 times more potent.