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Disruption of the substance P receptor (neurokinin‐1) gene does not prevent upregulation of preprotachykinin‐A mRNA in the spinal cord of mice following peripheral inflammation
Author(s) -
Palmer James A.,
De Felipe Carmen,
O'Brien John A.,
Hunt Stephen P.
Publication year - 1999
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1999.00771.x
Subject(s) - substance p , dynorphin , downregulation and upregulation , tachykinin receptor 1 , neurokinin a , hyperalgesia , neuropeptide , galanin , μ opioid receptor , medicine , receptor , tachykinin receptor , endocrinology , spinal cord , opioid peptide , nociception , biology , neuroscience , opioid , gene , biochemistry
The neuropeptide substance P is thought to play an important role in nociception, although the function of the peptide remains controversial. Following peripheral inflammation there is a pronounced upregulation of substance P expression both in sensory neurons and in postsynaptic neurons within the spinal cord. We have examined the levels of expression of mRNA encoding substance P and dynorphin following the development of inflammatory hyperalgesia in mice in which the substance P receptor gene, also known as the neurokinin‐1 receptor gene, has been disrupted by homologous recombination. We show that inflammatory hyperalgesia following injection of complete Freund's adjuvant develops normally in animals that lack the neurokinin‐1 receptor and that expression of mRNAs encoding substance P and the neuropeptide dynorphin are upregulated regardless of the genotype of the mouse. This suggests that substance P activity is not required for the development and maintenance of inflammatory hyperalgesia and that the upregulation of substance P expression is mediated by neurotransmitters other than substance P.