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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Updated: Dec 25, 2025

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
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Incomplete vesicular docking limits synaptic strength under high release probability conditions.

Gerardo Malagon1,2, Takafumi Miki1,3, Van Tran1

  • 1Université de Paris, SPPIN-Saints Pères Paris Institute for the Neurosciences, CNRS, Paris, France.

Elife
|April 2, 2020
PubMed
Summary
This summary is machine-generated.

Synaptic vesicle release at mammalian synapses saturates at 0.22 vesicles per site, not one, due to limited docked vesicle availability. Increasing external calcium concentration enhances this maximum synaptic output by increasing vesicle docking.

Keywords:
calcium concentrationneuroscienceratrelease sitesynapse

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biophysics

Background:

  • Central mammalian synapses utilize docking/release sites for synaptic vesicle exocytosis.
  • Previous assumptions suggested a maximum synaptic output of one vesicle per action potential per site.
  • Understanding the regulation of synaptic vesicle release is crucial for neural communication.

Purpose of the Study:

  • To investigate the maximum synaptic vesicle output per site at central mammalian synapses.
  • To determine the factors limiting synaptic output under conditions of increased calcium entry.
  • To evaluate the role of docked vesicle availability in synaptic transmission.

Main Methods:

  • Utilized deconvolution techniques to quantify synaptic vesicle output at single release sites.
  • Manipulated calcium entry using tetraethylammonium (TEA) in varying external calcium concentrations.
  • Applied current models of calcium-dependent exocytosis to interpret experimental results.

Main Results:

  • Synaptic output saturated at 0.22 vesicles per site, contradicting the one vesicle per site assumption.
  • This saturation limit was found to correlate with the probability of docking sites being occupied by vesicles at rest.
  • Increasing external calcium concentration from 1.5 mM to 3 mM increased maximum output to 0.47 vesicles per site, indicating enhanced docking site occupancy.

Conclusions:

  • Synaptic vesicle release is limited by the availability of docked vesicles at release sites.
  • The probability of vesicle docking, rather than calcium influx alone, dictates the maximum synaptic output.
  • External calcium concentration plays a significant role in regulating docking site occupancy and thus synaptic efficacy.