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Time-coded neurotransmitter release at excitatory and inhibitory synapses.

Authors
  • Rodrigues, Serafim1
  • Desroches, Mathieu2
  • Krupa, Martin2
  • Cortes, Jesus M3
  • Sejnowski, Terrence J4
  • Ali, Afia B5
  • 1 School of Computing and Mathematics, Plymouth University, Plymouth PL4 8AA, United Kingdom; , (United Kingdom)
  • 2 Inria Sophia Antipolis Mediterranee Research Centre, MathNeuro Team, 06902 Sophia Antipolis cedex, France; , (France)
  • 3 Biocruces Health Research Institute, Cruces University Hospital, 48903 Barakaldo, Bizkaia, Spain; Departamento de Biologia Celular e Histologia, University of the Basque Country, 48940 Leioa, Bizkaia, Spain; , (Spain)
  • 4 The Computational Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037; Howard Hughes Medical Institute, Salk Institute, La Jolla, CA 92037; Division of Biological Science, University of California, San Diego, La Jolla, CA 92093; [email protected]
  • 5 UCL School of Pharmacy, Department of Pharmacology, University College London, London WC1N 1AX, United Kingdom. , (United Kingdom)
Type
Published Article
Journal
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Publication Date
Feb 23, 2016
Volume
113
Issue
8
Identifiers
DOI: 10.1073/pnas.1525591113
PMID: 26858411
Source
Medline
Keywords
License
Unknown

Abstract

Communication between neurons at chemical synapses is regulated by hundreds of different proteins that control the release of neurotransmitter that is packaged in vesicles, transported to an active zone, and released when an input spike occurs. Neurotransmitter can also be released asynchronously, that is, after a delay following the spike, or spontaneously in the absence of a stimulus. The mechanisms underlying asynchronous and spontaneous neurotransmitter release remain elusive. Here, we describe a model of the exocytotic cycle of vesicles at excitatory and inhibitory synapses that accounts for all modes of vesicle release as well as short-term synaptic plasticity (STSP). For asynchronous release, the model predicts a delayed inertial protein unbinding associated with the SNARE complex assembly immediately after vesicle priming. Experiments are proposed to test the model's molecular predictions for differential exocytosis. The simplicity of the model will also facilitate large-scale simulations of neural circuits.

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