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 detailed molecular and cellular mechanisms underlying NREM and REM sleep in mammals are elusive. To address these challenges, we constructed a mathematical model, Averaged Neuron Model (AN Model), which recapitulates the electrophysiological characteristics of the slow-wave sleep. Comprehensive bifurcation analysis predicted that a Ca2+-dependent hyperpolarization pathway may play a role in slow-wave sleep. To experimentally validate this prediction, we generate and analyze 26 KO mice, and found that impaired Ca2+-dependent K+ channels, voltage-gated Ca2+ channels, or Ca2+/calmodulin-dependent kinases (Camk2a and Camk2b) decrease sleep duration, while impaired plasma membrane Ca2+ ATPase increases sleep duration. Genetical and pharmacological intervention and whole-brain imaging validated that impaired NMDA receptors reduce sleep duration and directly increase the excitability of cells. Based on these results, we propose phosphorylation hypothesis of sleep that phosphorylation-dependent regulation of Ca2+-dependent hyperpolarization pathway underlies the regulation of sleep duration in mammals. In this talk, I will also present how we identify essential genes (Chrm1 and Chrm3) in REM sleep regulation as well as new projects on human sleep/wake cycle measurements for next-generation sleep medicine and on whole-body/brain profiling of cells in mammals.