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Related Experiment Video

Updated: Feb 6, 2026

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A BDNF-Mediated Push-Pull Plasticity Mechanism for Synaptic Clustering.

Dragos Niculescu1, Kristin Michaelsen-Preusse2, Ülkü Güner2

  • 1Department of Synapse and Network Development, Netherlands Institute for Neuroscience, 1105 Amsterdam, the Netherlands; Department of Neurogenesis and Circuit Development, Vision Institute, 75012 Paris, France.

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|August 23, 2018
PubMed
Summary
This summary is machine-generated.

Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are crucial for synaptic clustering in developing neurons. This process refines neural networks by stabilizing synchronized synapses, guided by a push-pull mechanism involving BDNF and its precursor, proBDNF.

Keywords:
BDNFMMP9NMDARTrkBdevelopmenthippocampuspostsynapticproBDNFsynaptic clustering

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Activity-dependent synaptic plasticity refines neuronal networks during development.
  • Spontaneous neuronal activity facilitates synaptic clustering, enhancing brain computation.
  • Brain-derived neurotrophic factor (BDNF) and its receptor TrkB play roles in neuronal development and plasticity.

Purpose of the Study:

  • To investigate the role of TrkB activation and postsynaptic BDNF in synaptic clustering in developing hippocampal neurons.
  • To elucidate the mechanism by which BDNF/TrkB signaling influences synaptic transmission and clustering.
  • To explore the interplay between BDNF, proBDNF, and synaptic plasticity.

Main Methods:

  • Electrophysiological recordings in developing hippocampal neurons.
  • Manipulation of BDNF/TrkB signaling pathways.
  • Analysis of synaptic clustering and transmission properties.
  • Investigating the role of matrix-metalloproteinase-9 (MMP-9) and NMDA receptor activation.

Main Results:

  • TrkB activation and postsynaptic BDNF are essential for synaptic clustering in developing hippocampal neurons.
  • BDNF/TrkB signaling modulates synaptic transmission based on synapse clustering state, stabilizing synchronized synapses.
  • A push-pull plasticity mechanism involving BDNF and proBDNF regulates synaptic clustering.
  • Synaptic clustering requires MMP-9 activity for proBDNF to BDNF conversion.
  • NMDA receptor activation mediates out-of-sync depression upstream of proBDNF signaling.

Conclusions:

  • Endogenous BDNF/TrkB signaling stabilizes locally synchronized synapses, contributing to synaptic clustering.
  • A push-pull mechanism, with BDNF stabilizing clustered synapses and proBDNF downregulating unsynchronized synapses, refines neuronal networks.
  • This study reveals an efficient plasticity mechanism where proBDNF and mature BDNF establish synaptic clustering through antagonistic modulation of synaptic transmission.