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Atypical delayed paired-pulse depression at an identified synapse.

Michelle Sanchez-Rivera1, Montserrat G Cercós1, Citlali Trueta1

  • 1Departamento de Neurofisiología, Dirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México City, México.

The Journal of Physiology
|September 10, 2025
PubMed
Summary

We discovered a novel form of synaptic depression in leech neurons. This delayed depression, unlike typical forms, is calcium-dependent and not caused by vesicle depletion, suggesting a new plasticity mechanism.

Keywords:
anterior pagoda neurondelayed depressionleechpaired‐pulse depressionpressure‐sensory neuronsynaptic depressionsynaptic facilitationsynaptic plasticity

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Cellular Electrophysiology

Background:

  • Synaptic plasticity, including facilitation and depression, is modulated by stimulation patterns, presynaptic calcium, and vesicle pool dynamics.
  • Synaptic facilitation arises from calcium accumulation, while depression is typically linked to vesicle pool depletion.
  • Existing models struggle to explain all observed plasticity phenomena.

Purpose of the Study:

  • To investigate an unusual form of paired-pulse delayed depression at the synapse between pressure-sensitive and anterior pagoda neurons in the leech.
  • To elucidate the underlying mechanisms of this novel synaptic depression.
  • To propose a new model that accounts for the observed plasticity phenomena.

Main Methods:

  • Electrophysiological recordings of synaptic transmission between leech neurons.
  • Application of varying interstimulus intervals to induce facilitation and depression.
  • Experimental manipulation using EGTA-AM to probe calcium dependency.

Main Results:

  • Short interstimulus intervals (<700 ms) induced facilitation, consistent with residual calcium.
  • Long interstimulus intervals (>700 ms) produced a delayed depression, increasing with interval duration up to 1000 ms.
  • This delayed depression was reduced by EGTA-AM and did not correlate with vesicle depletion, deviating from classical models.

Conclusions:

  • A novel, calcium-dependent delayed synaptic depression mechanism exists, independent of vesicle pool depletion.
  • Classical models of synaptic plasticity are insufficient to explain these findings.
  • A new model involving a slow, calcium-dependent mechanism for vesicle removal from the readily releasable pool is proposed.