Prof John Wood FRS
-020 7679 6954 / j.wood@ucl.ac.uk

Molecular Nociception Group

Our research team focuses on genetic approaches to understanding the biology of damage-sensing neurons (nociceptors), somatosensation, pain and touch.
The past two decades have 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. Pain is still an enormous clinical problem, and new drugs are urgently required for a range of chronic pain syndromes.

Our group combines recombinant DNA technology, electrophysiology, gene targeting and behavioural approaches to explore the channels, receptors, transcription factors and regulatory pathways that control nociceptor excitability. We collaborate closely with human geneticists and clinicians, using mouse models to unravel molecular mechanisms that underlie pain disorders.  We also take part in early-stage drug discovery programmes based on targets we identify in the lab.

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. As well as providing information about pain pathways, the systems we study have a broad relevance to understanding how the nervous system works, in terms of synaptic plasticity, responses to environmental stimuli, sensation and behaviour. 

Selected publications

Cho H, Yang YD, Lee J, Lee B, Kim T, Jang Y, Back SK, Na HS, Harfe BD, Wang F, Raouf R, Wood JN, Oh U. The calcium-activated chloride channel anoctamin 1 acts as a heat sensor in nociceptive neurons. Nature Neurosci. 2012 May 27;15(7):1015-21.

Minett MS, Nassar MA, Clark AK, Passmore G, Dickenson AH, Wang F, Malcangio M Wood JN. Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons. Nature Comm. 2012, 3:791

Vetter I, Touska F, Hess A, Hinsbey R, Sattler S, Lampert A, Sergejeva M, Sharov A, Collins LS, Eberhardt M, Engel M, Cabot PJ, Wood JN, Vlachová V, Reeh PW, Lewis RJ, Zimmermann K. Ciguatoxins activate specific cold pain pathways to elicit burning pain from cooling. EMBO J. 2012 31(19):3795-808.

Chambers JC, Zhao J, Terracciano CM, Bezzina CR, Zhang W, Kaba R,            Navaratnarajah M, Lotlikar A, Sehmi JS, Kooner MK, Deng G, Siedlecka U, Parasramka S, El-Hamamsy I, Wass MN, Dekker LR, de Jong JS, Sternberg MJ, McKenna W, Severs NJ, de Silva R, Wilde AA, Anand P, Yacoub M, Scott J, Elliott P, Wood JN, Kooner JS. Genetic variation in SCN10A influences cardiac conduction. Nat Genet. 2010 Jan 10

Abrahamsen, B.,  Zhao J,  Asante C, Cendan C,  Marsh  S, Martinez-Barbera J , Nassar, MA, Dickenson AS and  J. N. Wood The cell and molecular basis of mechanical, cold and inflammatory pain. Science 321(5889):702-52007            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):855-8.

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.

Academic Career

Professor UCL

Wellcome foundation and Sandoz Institute – Group Leader

Visiting Professor Harvard, Seoul National University

Post Doc Institut Pasteur, St Georges Hospital

PhD Warwick 1976

Funding

MRC

Wellcome Trust

BBSRC

WCU Programme