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Presynaptic remodeling contributes to activity-dependent synaptogenesis.

Irina Nikonenko1, Pascal Jourdain, Dominique Muller

  • 1Department of Pharmacology, University Medical Center, 1211 Geneva 4, Switzerland.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 19, 2003
PubMed
Summary
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Short anoxia/hypoglycemia and theta burst stimulation promote presynaptic filopodia growth and synapse formation. Nitric oxide signaling, downstream of NMDA receptor activation, drives these rapid structural changes in presynaptic boutons.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Synaptic Plasticity

Background:

  • Synaptic plasticity, crucial for learning and memory, involves structural changes in both pre- and postsynaptic neurons.
  • Previous research linked dendritic filopodia and spine formation to plasticity, but presynaptic structural dynamics remained less understood.

Purpose of the Study:

  • To investigate the impact of plasticity-inducing conditions (anoxia/hypoglycemia, theta burst stimulation) on presynaptic structure.
  • To elucidate the molecular mechanisms, including calcium, NMDA receptors, and nitric oxide, underlying presynaptic remodeling.

Main Methods:

  • Confocal imaging of DiI-labeled axons
  • Electron microscopy
  • Stereological analyses
  • Three-dimensional reconstruction of axonal structures

Related Experiment Videos

Main Results:

  • Anoxia/hypoglycemia and theta burst stimulation induced rapid, calcium-dependent growth of presynaptic filopodia and varicosity remodeling.
  • Presynaptic filopodia formed new synapses with dendritic shafts and spines within 30 minutes.
  • NMDA receptor activation and nitric oxide signaling were essential for these presynaptic structural changes.

Conclusions:

  • Presynaptic structures exhibit rapid, activity-dependent plasticity, mirroring postsynaptic changes.
  • Presynaptic filopodia actively participate in synaptogenesis and spine formation.
  • A model involving NMDA receptor activation and nitric oxide release explains activity-dependent presynaptic growth.