On 28th November OxTalks will move to the new Halo platform and will become 'Oxford Events' (full details are available on the Staff Gateway).
There will be an OxTalks freeze beginning on Friday 14th November. This means you will need to publish any of your known events to OxTalks by then as there will be no facility to publish or edit events in that fortnight. During the freeze, all events will be migrated to the new Oxford Events site. It will still be possible to view events on OxTalks during this time.
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The HCN4 ion channel is well known for driving pacemaker activity in the heart and thus modulating the heart rate. The McNaughton lab has discovered that HCN2, a different member of the same family, plays a similar role in nerve fibres. When HCN2 is activated by inflammatory mediators released following tissue damage, then the firing of nerve action potentials is potentiated in nerve fibres which transmit the sensation of pain. Blocking the HCN2 ion channel may therefore provide analgesia, but blockers must be highly selective to avoid blocking the HCN4 ion channel which drives the heartbeat. We have found that HCN2-selective blockers can deliver remarkable analgesia in animal pain models, and thus may offer effective analgesia in poorly treated pain conditions such as neuropathic pain, an intractable pain condition caused by nerve damage. In more recent work we have found that HCN2 ion channels expressed in the auditory nerves may also be the drivers of tinnitus, another common and distressing condition associated with nerve damage.
