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Neural Plasticity
Volume 2016 (2016), Article ID 7607924, 30 pages
Research Article

Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study

1Department of Neurobiology, The University of Chicago, Chicago, IL 60637, USA
2Project-Team BEAGLE, INRIA Rhône-Alpes, 60097 Villeurbanne, France
3Departments of Statistics and Neurobiology, The University of Chicago, Chicago, IL 60637, USA

Received 5 January 2016; Accepted 15 February 2016

Academic Editor: Alfredo Pereira Jr.

Copyright © 2016 Maurizio De Pittà and Nicolas Brunel. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Glutamatergic gliotransmission, that is, the release of glutamate from perisynaptic astrocyte processes in an activity-dependent manner, has emerged as a potentially crucial signaling pathway for regulation of synaptic plasticity, yet its modes of expression and function in vivo remain unclear. Here, we focus on two experimentally well-identified gliotransmitter pathways, (i) modulations of synaptic release and (ii) postsynaptic slow inward currents mediated by glutamate released from astrocytes, and investigate their possible functional relevance on synaptic plasticity in a biophysical model of an astrocyte-regulated synapse. Our model predicts that both pathways could profoundly affect both short- and long-term plasticity. In particular, activity-dependent glutamate release from astrocytes could dramatically change spike-timing-dependent plasticity, turning potentiation into depression (and vice versa) for the same induction protocol.