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Author Notes:

Correspondence should be addressed to Peter Wenner, Department of Physiology, Room 601 Whitehead Bldg., Emory University School of Medicine, Atlanta, GA 30322. E-mail:pwenner@emory.edu.

M.A.G.-B., C.G.-I., C.L., and P.W. designed research.

M.A.G.-B., C.G.-I., C.L., and P.W. performed research.

M.A.G.-B., C.G.-I., C.L., and P.W. analyzed data.

M.A.G.-B., C.G.-I., C.L., and P.W. wrote the paper.

We thank Drs. Mark Rich and Astrid Prinz for valuable comments on the manuscript.

The authors declare no competing financial interests.

Subjects:

Research Funding:

This work was supported by grants from the National Institute of Neurological Disorders and Stroke and the Whitehall Foundation to P.W.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • chick embryo
  • homeostatic plasticity
  • nicotine
  • spinal cord
  • spontaneous release
  • synaptic scaling
  • METABOTROPIC GLUTAMATE RECEPTORS
  • HOMEOSTATIC PLASTICITY
  • RETINOIC ACID
  • DNA METHYLATION
  • MINIATURE NEUROTRANSMISSION
  • HIPPOCAMPAL-NEURONS
  • QUANTAL AMPLITUDE
  • AMPA RECEPTORS
  • INHIBITION
  • CHLORIDE

Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo

Tools:

Journal Title:

Journal of Neuroscience

Volume:

Volume 36, Number 27

Publisher:

, Pages 7268-7282

Type of Work:

Article | Final Publisher PDF

Abstract:

Homeostatic plasticity mechanisms maintain cellular or network spiking activity within a physiologically functional range through compensatory changes in synaptic strength or intrinsic cellular excitability. Synaptic scaling is one form of homeostatic plasticity that is triggered after blockade of spiking or neurotransmission in which the strengths of all synaptic inputs to a cell are multiplicatively scaled upward or downward in a compensatory fashion. We have shown previously that synaptic upscaling could be triggered in chick embryo spinal motoneurons by complete blockade of spiking or GABAA receptor (GABAAR) activation for 2 d in vivo. Here, we alter GABAAR activation in a more physiologically relevant manner by chronically adjusting presynaptic GABA release in vivo using nicotinic modulators or an mGluR2 agonist. Manipulating GABAAR activation in this way triggered scaling in a mechanistically similar manner to scaling induced by complete blockade of GABAARs. Remarkably, we find that altering action-potential (AP)-independent spontaneous release was able to fully account for the observed bidirectional scaling, whereas dramatic changes in spiking activity associated with spontaneous network activity had little effect on quantal amplitude. The reliance of scaling on an AP-independent process challenges the plasticity’s relatedness to spiking in the living embryonic spinal network. Our findings have implications for the trigger and function of synaptic scaling and suggest that spontaneous release functions to regulate synaptic strength homeostatically in vivo.

Copyright information:

© 2016 the authors.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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