Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
We have seen huge progress in our understanding as to how sensory neurons detect tissue injury and transmit this information to the central nervous system. This is critically dependent on a repertoire of ligand gated ion channels responding to thermal, mechanical and chemical stimuli and voltage gated ion channels which set excitability and are required for the generation of action potentials. Genetic variants in these same ion channels can lead to human Mendelian pain disorders which include the phenotypic extremes of both loss of pain and enhanced pain. The distinct clinical phenotypes can be related to the biophysical changes in channel function. We also recognise that variants in these same channels may contribute to the risk of more common acquired neuropathic pain disorders and pain perception at a population level. This knowledge has highlighted new analgesic drug targets and the development of new treatments as well as a more personalised pain medicine approach.
