Alterations in neurokinin 1 receptor gene expression in models of pain and inflammation

Can J Physiol Pharmacol. 1995 Jul;73(7):854-9. doi: 10.1139/y95-117.


Substance P and the related tachykinin peptides are involved in inflammatory processes and in the transmission of sensory nociceptive information. In this article we review the evidence implicating substance P and the neurokinin 1 (NK1) receptor in arthritic disease. We also provide preliminary evidence demonstrating that cultured synoviocytes from a patient with rheumatoid arthritis express NK1 receptor mRNA that can be downregulated by tumor necrosis factor alpha, whereas synoviocytes from a normal patient do not express detectable NK1 receptor mRNA or protein. Data are also presented summarizing recent studies on nociception-induced increases in sensory ganglia of levels of mRNA encoding substance P and increases in dorsal horn NK1 receptor mRNA levels. Morphine pretreatment blocked the increases in dorsal horn NK1 receptor mRNA levels but did not block the nociception-induced substance P encoding mRNA levels in sensory ganglia. These results are discussed with reference to mechanisms that may regulate P turnover and NK1 receptor sensitivity in models of pain and inflammation.

Publication types

  • Review

MeSH terms

  • Animals
  • Arthritis, Rheumatoid / metabolism*
  • Gene Expression Regulation*
  • Humans
  • Pain / metabolism*
  • Receptors, Neurokinin-1 / genetics*
  • Receptors, Neurokinin-1 / physiology
  • Substance P / genetics
  • Substance P / physiology


  • Receptors, Neurokinin-1
  • Substance P