Close
Professor David Bennett
WIBR Seminar
'The role of potassium channel expression and trafficking in human neuropathic pain'
Professor David Bennett
Professor of neurology and neurobiology,
Nuffield department of clinical neurosciences,
Senior Wellcome Clinical Scientist,
Honorary consultant neurologist
University of Oxford
Host: Professor John Wood
Neuropathic pain following peripheral nerve injury is associated with spontaneous activity in damaged myelinated sensory axons which begins to normalise over time. Using rodent models and human tissue we investigated the composition and distribution of shaker type potassium channels (Kv1 channels) within myelinated sensory axons following injury. These potassium channels act as 'breaks' on excitability and are normally localised to the juxtaparanodal domain. Both at the neuroma but also in the proximal axon we found that the sub-unit composition and the distribution of these potassium channels changed following nerve injury. Electrophysiological and behavioural assessment demonstrates that these changes are a protective mechanism to suppress hyper-excitability post injury.
Kv channels form a macro-molecular complex with CASPR2 which is critical for their trafficking. Auto-antibodies to CASPR2 have recently been linked to the development of neuropathic pain in humans. I will discuss how CASPR2 has an important role in regulating primary afferent excitability through its interaction with Kv channels and the development of a new model to study these auto-antibodies in vivo. Both of these lines of evidence suggest that both sub-type expression and importantly the trafficking of Kv channels have key roles in the development of primary afferent hyper-excitability and neuropathic pain.
Date: Thursday 21st April 2016
Time: 4pm (please arrive 15 mins before start)
Venue: Cruciform Café, 1st Floor Cruciform Building, Gower Street, UCL, WC1E 6BT
Refreshments will be provided
Download poster