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Related Experiment Videos

Physiological activity depresses synaptic function through an effect on vesicle priming.

Krista L Moulder1, Xiaoping Jiang, Amanda A Taylor

  • 1Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|June 16, 2006
PubMed
Summary
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Neurons adapt glutamate release through persistent presynaptic changes, maintaining firing rates. This adaptation, driven by electrical activity, involves vesicle priming, not vesicle pool size.

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Cellular Electrophysiology

Background:

  • Neurons maintain stable firing rates through homeostatic synaptic plasticity.
  • Presynaptic adaptation is a key mechanism for regulating neuronal excitability.

Purpose of the Study:

  • To investigate the induction and characteristics of persistent presynaptic adaptation in hippocampal pyramidal neurons.
  • To explore how changes in electrical activity influence glutamate release and synaptic function.

Main Methods:

  • Mild extracellular potassium elevation to induce depolarization.
  • FM1-43 staining and vesicular glutamate transporter-1 (VGLUT1) antibody staining to assess synapse activity.
  • Tetrodotoxin (TTX) and postsynaptic receptor blockade to probe adaptation mechanisms.

Related Experiment Videos

  • Electrophysiological recordings to measure excitatory postsynaptic currents (EPSCs) and readily releasable pool (RRP) size.
  • Alpha-latrotoxin stimulation to assess vesicle release.
  • Ultrastructural analysis of synaptic vesicles.

    • Main Results:

    • Mild depolarization over days led to glutamate release adaptation, indicated by a mismatch between active and total synapses.
    • Adaptation was all-or-none, with no change in recycling vesicle pool size at active synapses.
    • Tetrodotoxin (TTX) reversed adaptation, suggesting spiking activity normally maintains a fraction of inactive terminals.
    • Chronic depolarization and electrical stimulation reduced RRP size, confirming spiking-induced adaptation.
    • Ultrastructural studies showed no changes in vesicle numbers, but alpha-latrotoxin experiments suggested altered vesicle priming.

    Conclusions:

    • Glutamatergic neurotransmission persistently adapts to altered electrical activity within a physiological range.
    • Presynaptic adaptation involves changes in vesicle priming rather than alterations in the total vesicle pool.
    • Neuronal firing activity plays a crucial role in maintaining synaptic homeostasis by regulating presynaptic release probability.