Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study.

dc.contributor.author

De Pittà, Maurizio

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Brunel, Nicolas

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2021-06-06T16:22:47Z

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2021-06-06T16:22:47Z

dc.date.issued

2016-01

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2021-06-06T16:22:40Z

dc.description.abstract

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.

dc.identifier.issn

2090-5904

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1687-5443

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https://hdl.handle.net/10161/23355

dc.language

eng

dc.publisher

Hindawi Limited

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Neural plasticity

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10.1155/2016/7607924

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Hippocampus

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Astrocytes

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Synapses

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Animals

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Glutamic Acid

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Synaptic Transmission

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Neuronal Plasticity

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Models, Neurological

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Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study.

dc.type

Journal article

pubs.begin-page

7607924

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School of Medicine

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Physics

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Neurobiology

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Duke Institute for Brain Sciences

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Center for Cognitive Neuroscience

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Duke

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Trinity College of Arts & Sciences

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Basic Science Departments

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University Institutes and Centers

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Institutes and Provost's Academic Units

pubs.publication-status

Published

pubs.volume

2016

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