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SUMMARY:Why do neurons spike spontaneously? - Tim Vogels (University of Ox
 ford)
DTSTART:20200427T153000Z
DTEND:20200427T163000Z
UID:TALK141952@talks.cam.ac.uk
CONTACT:Jake Stroud
DESCRIPTION:Zoom information:\n\nLink: https://us02web.zoom.us/j/991762764
 71?pwd=c0RtbFpSUGNOUTgrUjJPZWxHN1pJdz09\n\nMeeting ID: 991 7627 6471\n\nPa
 ssword: 314708\n\nTalk abstract:\nSpontaneous firing\, observed in many ne
 urons\, is often attributed to ion channel or network level noise. Cortica
 l cells during slow wave sleep exhibit transitions between so called Up an
 d Down states. In this sleep state\, with limited sensory stimuli\, neuron
 s fire in the Up state. Spontaneous firing is also observed in slices of c
 holinergic interneurons\, cerebellar Purkinje cells and even brainstem ins
 piratory neurons. In such in vitro preparations\, where the functional rel
 evance is long lost\, neurons continue to display a rich repertoire of fir
 ing properties. It is perplexing that these neurons\, instead of saving th
 eir metabolic energy during information downtime and functional irrelevanc
 e\, are eager to fire. We propose that spontaneous firing is not a chance 
 event but instead\, a vital activity for the well-being of a neuron. Neuro
 ns in anticipation of synaptic inputs\, keep their ATP levels at maximum. 
 As recovery from inputs requires most of the energy resources\, neurons ar
 e ATP surplus and ADP scarce during synaptic quiescence. With ADP as the r
 ate-limiting step\, ATP production stalls in the mitochondria. This leads 
 to toxic Reactive Oxygen Species (ROS) formation\, which are known to disr
 upt many cellular processes. We hypothesize that spontaneous firing occurs
  at these conditions as a release valve to spend energy and to restore ATP
  production\, shielding against ROS. By linking a mitochondrial metabolism
  model to a conductance-based neuron model\, we show that spontaneous firi
 ng depends on baseline ATP usage and on ATP-cost-per-spike. From our model
 \, emerges a mitochondrial mediated homeostatic mechanism that provides a 
 recipe for different firing patterns. Our findings\, though mostly affecti
 ng intracellular dynamics\, may have large knock-on effects on the nature 
 of neural coding. Hitherto it has been thought that the neural code is opt
 imised for energy minimisation\, but this may be true only when neurons do
  not experience synaptic quiescence.
LOCATION:Online on Zoom
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