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Publication : Inhibition of inflammation and hyperalgesia in NK-1 receptor knock-out mice.

First Author  Kidd BL Year  2003
Journal  Neuroreport Volume  14
Issue  17 Pages  2189-92
PubMed ID  14625445 Mgi Jnum  J:103700
Mgi Id  MGI:3610631 Doi  10.1097/00001756-200312020-00011
Citation  Kidd BL, et al. (2003) Inhibition of inflammation and hyperalgesia in NK-1 receptor knock-out mice. Neuroreport 14(17):2189-92
abstractText  We sought to characterise the contribution of the neuropeptide substance P to the outcome of two models of footpad inflammation of differing severity. In an intense inflammatory model produced by intra-plantar Mycobacterium tuberculosus (10 mg/ml) substantial reductions in footpad swelling, histological outcome and mechanical hyperalgesia were observed from early time points in mice lacking the neurokin-1 receptor for substance P compared with wild-type controls. Conversely, in a less intense model (M. tuberculosus 1 mg/ml) no differences were observed other than for a reduction in mechanical hyperalgesia at later time points (day 9 onwards). The results point to a previously unrecognised influence of substance P on peripheral tissue injury and the maintenance of hyperalgesia during more severe or more chronic phases of inflammatory disease.
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