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REST-Dependent Presynaptic Homeostasis Induced by Chronic Neuronal Hyperactivity.

F Pecoraro-Bisogni1,2, Gabriele Lignani3,4, A Contestabile2

  • 1Department of Experimental Medicine, Section of Physiology, University of Genova, Viale Benedetto XV 3, 16132, Genoa, Italy.

Molecular Neurobiology
|August 9, 2017
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Summary
This summary is machine-generated.

The study reveals that REST, a transcriptional repressor, downscales both neuronal intrinsic excitability and presynaptic efficiency. This molecular player is crucial for neuronal homeostasis during chronic hyperactivity.

Keywords:
Excitatory synapseGene transcriptionHomeostatic plasticityNeuronal excitabilityPresynaptic terminalsRESTSynaptic vesicles

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Biology

Background:

  • Homeostatic plasticity balances neuronal activity through synaptic strength or intrinsic excitability adjustments.
  • A unified molecular model for these distinct homeostatic processes is currently lacking.
  • REST was previously identified as critical for downscaling intrinsic excitability in response to hyperactivity.

Purpose of the Study:

  • To investigate REST's role in synaptic homeostasis.
  • To determine if REST influences synaptic strength during neuronal hyperactivity.
  • To elucidate the molecular mechanisms underlying REST-mediated synaptic plasticity.

Main Methods:

  • Utilized cultured hippocampal neurons subjected to prolonged elevated electrical activity.
  • Investigated REST's effect on excitatory synapse strength.
  • Analyzed changes in synaptic vesicle pool size.
  • Examined transcriptional and translational regulation of presynaptic REST target genes.

Main Results:

  • REST reduces excitatory synapse strength at the presynaptic level.
  • Chronic hyperactivity leads to a REST-dependent decrease in synaptic vesicle pool size.
  • This decrease is mediated by transcriptional and translational repression of presynaptic REST target genes.

Conclusions:

  • REST is a key molecular player in neuronal homeostasis.
  • REST simultaneously downscales intrinsic excitability and presynaptic efficiency in response to hyperactivity.
  • REST mediates activity-dependent transcriptional regulation of homeostatic plasticity.