Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X3 receptors

Veronika Souslova, Paolo Cesare, Yanning Ding, Armen N. Akopian, Louise Stanfa, Rie Suzuki, Katherine Carpenter, Anthony Dickenson, Susan Boyce, Ray Hill, Daniela Nebenius-Oosthuizen, Andrew J.H. Smith, Emma J. Kidd, John N. Wood

Research output: Contribution to journalArticlepeer-review

401 Scopus citations


ATP activates damage-sensing neurons (nociceptors) and can evoke a sensation of pain. The ATP receptor P2X3 is selectively expressed by nociceptors and is one of seven ATP-gated, cation-selective ion channels. Here we demonstrate that ablation of the P2X3 gene results in the loss of rapidly desensitizing ATP-gated cation currents in dorsal root ganglion neurons, and that the responses of nodose ganglion neurons to ATP show altered kinetics and pharmacology resulting from the loss of expression of P2X(2/3) heteromultimers. Null mutants have normal sensorimotor function. Behavioural responses to noxious mechanical and thermal stimuli are also normal, although formalin-induced.

Original languageEnglish (US)
Pages (from-to)1015-1017
Number of pages3
Issue number6807
StatePublished - Oct 26 2000
Externally publishedYes

ASJC Scopus subject areas

  • General


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