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John Wood

WIBR Department of Medicine


We are interested in peripheral pain pathways and the afferent and efferent functions of sensory neurons, particularly those that respond to tissue damage (nociceptors). We examine mechanisms by first mapping, then mimicking, human monogenic pain syndromes (gain or loss of function) in transgenic mice. At present we are GCaMP-imaging live mice to define modality-specific sets of sensory neurons and characterise their transcriptomes with RNAseq. We then use pain models to look at changes in gene expression associated with chronic pain in order to define new analgesic drug targets. In addition, we are cataloguing the mechano-transducers involved in innocuous and noxious mechanosensation. We collaborate with groups in Harvard, Zurich, Karolinska and Cambridge, as well as a range of Pharma and start-up companies on pain mechanisms.


A number of possible projects exist at the moment:

  • Sodium as a second messenger; how does a sodium channel (Nav1.7) regulate GPCR activity and transcription of opioid peptides?
  • Mechanisms of mechano-transduction in nociceptors.
  • Genetic definition of subsets of sensory neurons and their role in distinct pain mechanisms.
  • Mapping new loss of function human heritable pain conditions and examining underlying mechanisms.

Candidates would obtain a strong training in the application of recombinant DNA technology, transgenic mouse production and behavioural characterisation, as well as state of the art imaging and electrophysiology as applied to neurobiological problems.


Emery EC, et al. Distinct sets of somatosensory neurons respond to mechanical, cold and heat stimuli in vivo. Science Advances, in Press 2016.

Minett MS, et al. Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7. Nat Comms. 2015 Dec 4;6:8967

Ranade SS, et al. Piezo2 is the major transducer of mechanical forces for touch sensation in mice. Nature. 2014 Dec 4;516(7529):121-5