Temporal Coding-Induced Synaptic Plasticity Determines Clock-Driven Sleep Quality
Neurons use two fundamental coding schemes to convey information: rate coding (frequency of firing) and temporal coding (timing of firing). Although temporal coding has long been postulated to be important for encoding responses to stimuli or internal states, this hypothesis has been challenging to test. I will describe how the circadian clock acts via a novel clock output molecule, Wide Awake (WAKE), to tune biophysical properties of spikes to induce regular firing of specific clock neurons at night. Optogenetic experiments demonstrate that these changes in the pattern of firing, in the absence of changes in firing rate, directly alter sleep quality. Computational modeling shows that the rhythmic changes in ionic flux driven by WAKE are sufficient to account for both the dynamic modulation of spike morphology and the regularity of the spike train. Finally, I will show how temporal coding in these clock neurons is transformed to rate coding changes in downstream arousal neurons and demonstrate that temporal coding alone can induce synaptic plasticity that encodes persistent changes in clock-regulated sleep quality.
Date: 12 April 2018, 12:00 (Thursday, -1st week, Trinity 2018)
Venue: Oxford Martin School, 34 Broad Street OX1 3BD
Venue Details: 34 Broad Street, Oxford
Speaker: Dr Mark Wu (Johns Hopkins University)
Organising department: Department of Physiology, Anatomy and Genetics (DPAG)
Organiser: Fiona Woods (University of Oxford, Department of Physiology Anatomy and Genetics, Centre for Neural Circuits and Behaviour)
Organiser contact email address: fiona.woods@cncb.ox.ac.uk
Part of: CNCB Seminar Series
Booking required?: Not required
Audience: Members of the University only
Editor: Fiona Woods