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The proportion of TRPV1 protein-positive lumbar DRG neurones does not increase in the course of acute and chronic antigen-induced arthritis in the knee joint of the rat.

Abstract
The TRPV1 receptor, previously called VR1 receptor, is a non-selective cation channel gated by capsaicin, noxious heat, protons and anandamide. The TRPV1 receptor is essential for the development of thermal hyperalgesia. The present study investigated whether the proportion of neurones with TRPV1 receptor increases in lumbar DRG neurones in the course of an antigen-induced arthritis (AIA) of one knee joint in the rat. In control rats 38.1+/-2.3% of the neurones from sections of the L1-L5 ganglia showed TRPV1-like immunoreactivity. Neither in the acute (3 days) nor chronic phase (21 days) of AIA in the knee joint the proportion of TRPV1-like immunoreactive profiles showed significant changes. Thus AIA in the knee joint is not associated with an up-regulation of the TRPV1 receptor in the lumbar DRG neurones.
AuthorsKarl-Jürgen Bär, Hans-Georg Schaible, Rolf Bräuer, Karl-Jürgen Halbhuber, Gisela Segond von Banchet
JournalNeuroscience letters (Neurosci Lett) Vol. 361 Issue 1-3 Pg. 172-5 (May 06 2004) ISSN: 0304-3940 [Print] Ireland
PMID15135921 (Publication Type: Journal Article)
Chemical References
  • Antigens
  • Inflammation Mediators
  • Receptors, Drug
  • methylated bovine serum albumin
  • Serum Albumin, Bovine
Topics
  • Acute Disease
  • Animals
  • Antigens
  • Arthralgia (chemically induced, metabolism, physiopathology)
  • Arthritis, Experimental (chemically induced, metabolism, physiopathology)
  • Cell Count
  • Disease Models, Animal
  • Female
  • Ganglia, Spinal (cytology, metabolism)
  • Hyperalgesia (chemically induced, metabolism, physiopathology)
  • Inflammation Mediators
  • Knee Joint (innervation, physiopathology)
  • Lumbosacral Region
  • Neurons, Afferent (cytology, metabolism)
  • Nociceptors (cytology, metabolism)
  • Rats
  • Rats, Inbred Lew
  • Receptors, Drug (metabolism)
  • Serum Albumin, Bovine
  • Up-Regulation (drug effects, physiology)

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