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SUMMARY:Why do neurons spike spontaneously? - Tim Vogels (University of Ox
 ford)
DTSTART:20200427T153000Z
DTEND:20200427T163000Z
UID:TALK141949@talks.cam.ac.uk
CONTACT:Jake Stroud
DESCRIPTION:Zoom information:\nLink: https://us02web.zoom.us/j/99176276471
 ?pwd=c0RtbFpSUGNOUTgrUjJPZWxHN1pJdz09\nMeeting ID: 991 7627 6471\nPassword
 : 314708\n\nTalk abstract:\nSpontaneous firing\, observed in many neurons\
 , is often attributed to ion channel or network level noise. Cortical cell
 s during slow wave sleep exhibit transitions between so called Up and Down
  states. In this sleep state\, with limited sensory stimuli\, neurons fire
  in the Up state. Spontaneous firing is also observed in slices of choline
 rgic interneurons\, cerebellar Purkinje cells and even brainstem inspirato
 ry neurons. In such in vitro preparations\, where the functional relevance
  is long lost\, neurons continue to display a rich repertoire of firing pr
 operties. It is perplexing that these neurons\, instead of saving their me
 tabolic energy during information downtime and functional irrelevance\, ar
 e 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. Neurons in 
 anticipation of synaptic inputs\, keep their ATP levels at maximum. As rec
 overy from inputs requires most of the energy resources\, neurons are ATP 
 surplus and ADP scarce during synaptic quiescence. With ADP as the rate-li
 miting step\, ATP production stalls in the mitochondria. This leads to tox
 ic Reactive Oxygen Species (ROS) formation\, which are known to disrupt ma
 ny cellular processes. We hypothesize that spontaneous firing occurs at th
 ese conditions as a release valve to spend energy and to restore ATP produ
 ction\, shielding against ROS. By linking a mitochondrial metabolism model
  to a conductance-based neuron model\, we show that spontaneous firing dep
 ends on baseline ATP usage and on ATP-cost-per-spike. From our model\, eme
 rges a mitochondrial mediated homeostatic mechanism that provides a recipe
  for different firing patterns. Our findings\, though mostly affecting int
 racellular dynamics\, may have large knock-on effects on the nature of neu
 ral coding. Hitherto it has been thought that the neural code is optimised
  for energy minimisation\, but this may be true only when neurons do not e
 xperience synaptic quiescence.
LOCATION:Online on Zoom
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