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Wellcome Trust conference The Challenges of Chronic Pain

11-13 March 2015
Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

Abstract deadline: 30 January 2015
Registration deadline: 16 February 2015

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Past Research
Tissue-specific and inducible knock-outs
We manipulate genes in mice to understand more about pain pathways. Many broadly expressed genes are involved in a variety of physiological processes, and so specific drugs (of which there are few) or conventional gene deletion techniques are not particularly informative about the specific role of a gene product in a defined physiological process. By deleting genes only in nociceptive neurons, we can unravel the contribution of a gene product to pain induction without complications from effects on other organ systems or the central nervous system. At the moment we are using a Cre-recombinase mouse expressed only in nociceptors to delete the voltage-gated sodium channel gene encoding PN1 (Nav1.7). Electrophysiology and behavioral studies are now allowing us to define the role of Nav1.7 in inflammatory and neuropathic pain. This system is applicable to any gene of interest, and is being extended by the use of mice that express Cre in proprioreceptive and touch sensitive neurons, as well as by the use of drug-inducible Cre mice. Participation in the European mouse phenotyping project, (Eumorphia) also allows us to examine comprehensively other phenotypic effects of sensory neuron gene deletion.


1999 Akopian, A.N. et al. The tetrodotoxin-resistant sodium channel SNS plays a specialized role in pian pathways. Nature Neuroscience 2, 541-548.
2000 Souslova, V. et al. Warm-coding deficits and aberrant inflammotory pain in mice lacking P2X3 receptors. Nature 407(6807):1015-7.
2001 Metzger, D, Chambon P. Site- and time-specific gene targeting gene targeting in the mouse. Methods. 24(1):71-80.

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