Department of Biology, Medawar Building, University College London, Gower Street, London WC1E 6BT, UK

Research focus

Selected publications

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Research Focus

Based in the Department of Biology, the Molecular Nociception Group focuses on genetic approaches to understanding the biology of damage-sensing neurons, somatosensation, pain  and touch The past decade has seen a revolution in our understanding of the receptor systems and regulatory pathways that underlie the responses of these specialised cells to the occurrence of tissue damage. This has important implications for human health and disease.

Our group combines recombinant DNA technology, electrophysiology and gene targeting and behavioural approaches to explore the channels, receptors, transcription factors and regulatory pathways that control nociceptor excitability. UCL provides an exciting environment for basic neuroscience and clinical interactions.

We collaborate with research groups in Europe, the United States, Korea, Japan and Australia, using transgenic mouse models, natural products and cloned genes to explore the physiology of pain perception. The systems we study have a broad relevance to understanding how the nervous system works, in terms of synaptic plasticity, responses to environmental stimuli and sensation and behaviour.
 

Prof. John N Wood is head of the Molecular Nociception Group and a member of the London Pain Consortium.

Click here to contact Prof. Wood for further information

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Selected Publications

Zimmermann K, Leffler A, Babes A, Cendan CM, Carr RW, Kobayashi J, Nau C, Wood JN, Reeh PW. Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures. Nature. 2007 Jun 14;447(7146):856-9.

Drew LJ, Rugiero F, Cesare P, Gale JE, Abrahamsen B, Bowden S, Heinzmann S, Robinson M, Brust A, Colless B, Lewis RJ, Wood JN. High-threshold mechanosensitive ion channels blocked by a novel conopeptide mediate pressure-evoked pain. PLoS ONE. 2007 Jun 13;2:e5151.

Drew LJ, Wood JN. FM1-43 is a permeant blocker of mechanosensitive ion channels in sensory neurons and inhibits behavioural responses to mechanical stimuli Mol Pain. 2007 Jan 6;3:1.

Cox JJ, Reimann F, Nicholas AK, Thornton G, Roberts E, Springell K, Karbani G, Jafri H, Mannan J, Raashid Y, Al-Gazali L, Hamamy H, Valente EM, Gorman S, Williams R, McHale DP, Wood JN, Gribble FM, Woods CG. An SCN9A channelopathy causes congenital inability to experience pain. Nature. 2006 Dec 14;444(7121):894-8.

Fertleman CR, Baker MD, Parker KA, Moffatt S, Elmslie FV, Abrahamsen B, Ostman J, Klugbauer N, Wood JN, Gardiner RM, Rees M. SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron. 2006 Dec 7;52(5):767-74.

Ekberg J, Jayamanne A, Vaughan CW, Aslan S, Thomas L, Mould J, Drinkwater R, Baker MD, Abrahamsen B, Wood JN, Adams DJ, Christie MJ, Lewis RJ. muO-conotoxin MrVIB selectively blocks Nav1.8 sensory neuron specific sodium channels and chronic pain behavior without motor deficits. Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):17030-5.

Nassar MA, Baker MD, Levato A, Ingram R, Mallucci G, McMahon SB, Wood JN. Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice. Mol Pain. 2006 Oct 19;2:33.

Foulkes T, Nassar MA, Lane T, Matthews EA, Baker MD, Gerke V, Okuse K, Dickenson AH, Wood JN. Deletion of annexin 2 light chain p11 in nociceptors causes deficits in somatosensory coding and pain behavior. J Neurosci. 2006 Oct 11;26(41):10499-507.

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Molecular Nociception Group, last updated 17/07/2007