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 and John N. Wood ()
Additional contact information
Veronika Souslova: Department of Biology
Paolo Cesare: Department of Biology
Yanning Ding: Department of Biology
Armen N. Akopian: Department of Biology
Louise Stanfa: University College London
Rie Suzuki: University College London
Katherine Carpenter: University College London
Anthony Dickenson: University College London
Susan Boyce: Merck Sharp and Dohme Research Labs
Ray Hill: Merck Sharp and Dohme Research Labs
Daniela Nebenius-Oosthuizen: Centre for Genome Research, Edinburgh University
Andrew J.H. Smith: Centre for Genome Research, Edinburgh University
Emma J. Kidd: Welsh School of Pharmacy, Cardiff University
John N. Wood: Department of Biology

Nature, 2000, vol. 407, issue 6807, 1015-1017

Abstract: Abstract ATP activates damage-sensing neurons (nociceptors) and can evoke a sensation of pain1. The ATP receptor P2X3 is selectively expressed by nociceptors2,3 and is one of seven ATP-gated, cation-selective ion channels4,5,6. 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 P2X2/3 heteromultimers. Null mutants have normal sensorimotor function. Behavioural responses to noxious mechanical and thermal stimuli are also normal, although formalin-induced pain behaviour is reduced. In contrast, deletion of the P2X3 receptor causes enhanced thermal hyperalgesia in chronic inflammation. Notably, although dorsal-horn neuronal responses to mechanical and noxious heat application are normal, P2X3-null mice are unable to code the intensity of non-noxious ‘warming’ stimuli.

Date: 2000
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DOI: 10.1038/35039526

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