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A subthreshold synaptic mechanism regulating BDNF expression and resting synaptic strength.

Patricia M Horvath1, Natali L Chanaday2, Baris Alten3

  • 1Department of Pharmacology, Vanderbilt University, Nashville, TN 37235, USA; Department of Neuroscience, the University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

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|August 4, 2021
PubMed
Summary
This summary is machine-generated.

Spontaneous inhibitory neurotransmission regulates brain-derived neurotrophic factor (BDNF) gene transcription and synaptic plasticity. Blocking inhibitory events increases BDNF, impacting synaptic strength at rest.

Keywords:
BDNFGABANpas4activity-induced geneinhibitioninhibitory neurotransmissionspontaneous neurotransmissionsynaptic scalingsynaptic transmissiontranscription

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Protein translation is regulated by spontaneous excitatory neurotransmission.
  • The effect of spontaneous neurotransmitter release on gene transcription is not well understood.

Purpose of the Study:

  • To investigate how spontaneous inhibitory and excitatory neurotransmission balance affects brain-derived neurotrophic factor (BDNF) regulation and synaptic plasticity.
  • To elucidate the role of spontaneous neurotransmission in gene transcription and synaptic strength.

Main Methods:

  • Studied the effects of blocking spontaneous inhibitory events on gene transcription (Bdnf, Npas4).
  • Investigated the role of calcium signaling, NMDA receptors (NMDARs), and L-type voltage-gated calcium channels (VGCCs).
  • Manipulated spontaneous inhibitory and excitatory currents to assess their impact on transcription and synaptic strength.

Main Results:

  • Blocking spontaneous inhibitory events increased Bdnf and Npas4 transcription via altered calcium signaling, reversible by NMDAR or VGCC antagonism.
  • Transcription was bidirectionally altered by spontaneous inhibitory currents, but not excitatory ones.
  • Blocking spontaneous inhibitory events caused multiplicative downscaling of excitatory synaptic strength, dependent on transcription and BDNF signaling.

Conclusions:

  • Spontaneous inhibitory neurotransmission plays a crucial role in BDNF signaling.
  • This signaling pathway at rest sets the overall excitatory synaptic strength.
  • Findings reveal a novel mechanism regulating synaptic plasticity and gene expression.