This report was presented at The Journal of Physiology Symposium on Ion Channels: Their Structure, Function and Control, Fukuoka, Kyushu, Japan, 24 March 2003. It was commissioned by the Editorial Board and reflects the views of the author.
P2X3 receptors and peripheral pain mechanisms
Article first published online: 12 JAN 2004
The Journal of Physiology
Volume 554, Issue 2, pages 301–308, January 2004
How to Cite
North, R. A. (2004), P2X3 receptors and peripheral pain mechanisms. The Journal of Physiology, 554: 301–308. doi: 10.1113/jphysiol.2003.048587
- Issue published online: 12 JAN 2004
- Article first published online: 12 JAN 2004
- (Received 4 June 2003; accepted after revision 25 June 2003; first published online 27 June 2003)
ATP released from damaged or inflamed tissues can act at P2X receptors expressed on primary afferent neurones. The resulting depolarization can initiate action potentials that are interpreted centrally as pain. P2X3 subunits are found in a subset of small-diameter, primary afferent neurones, some of which are also sensitive to capsaicin. They can form homo-oligomeric channels, or they can assemble with P2X2 subunits into hetero-oligomers. Studies with antagonists selective for P2X3-containing receptors, experiments with antisense oligonucleotides to reduce P2X3 subunit levels, and behavioural testing of P2X3 knock-out mice, all suggest a role for the P2X2/3 receptor in the signalling of chronic inflammatory pain and some features of neuropathic pain. The availability of such tools and experimental approaches promises to accelerate our understanding of the other physiological roles for P2X receptors on primary afferent neurones.