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Competition between phasic and asynchronous release for recovered synaptic vesicles at developing hippocampal

Yo Otsu1, Vahid Shahrezaei, Bo Li

  • 1Kinsmen Laboratory and Brain Research Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|January 16, 2004
PubMed
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During high-frequency stimulation, neurons shift from phasic to asynchronous neurotransmitter release. This asynchronous release maintains synaptic transmission by utilizing readily releasable pools of quanta.

Area of Science:

  • Neuroscience
  • Synaptic Transmission
  • Cellular Physiology

Background:

  • Developing hippocampal neurons exhibit rapid depression of evoked synaptic activity during high-frequency stimulation.
  • Evoked (phasic) excitatory synaptic release is attenuated by repeated stimuli.

Purpose of the Study:

  • To investigate the mechanisms underlying synaptic transmission during sustained stimulation.
  • To elucidate the roles of phasic and asynchronous release in maintaining neuronal communication.

Main Methods:

  • Utilized microisland cultures of developing hippocampal neurons.
  • Applied 1-second trains of 20 Hz stimulation.
  • Investigated neurotransmitter release using sucrose-induced depletion and EGTA-AM.
  • Employed computational modeling to analyze release dynamics.

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Main Results:

  • Asynchronous release persisted at a high rate (approx. 2.8 RRPs/sec) and was resistant to RRP depletion.
  • Phasic and asynchronous release competed for a common pool of release-ready quanta.
  • Blocking asynchronous release enhanced steady-state phasic release.
  • Prolonging asynchronous release delayed phasic release recovery.
  • Modeling indicated asynchronous release out-competes phasic release for recovered quanta due to sustained bulk intracellular Ca2+.

Conclusions:

  • Synaptic transmission is maintained during train stimulation by a switch to asynchronous release.
  • Asynchronous release leverages sustained bulk intracellular Ca2+ ([Ca2+]i) to sustain transmission.
  • Phasic release, triggered by brief Ca2+ microdomains, is less effective during sustained stimulation when asynchronous release is active.