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	    2016</a> | <a href="http://www.inria.fr/en/teams/beagle">Presentation of the Project-Team BEAGLE</a> | <a href="http://team.inria.fr/beagle/">BEAGLE Web Site
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        <h2>Section: 
      New Results</h2>
        <h3 class="titre3">Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission</h3>
        <p>Participants: M. De Pittà in collaboration with N. Brunel, Dept of Neuroscience and Statistics, University of Chicago, USA.</p>
        <p>Glutamatergic gliotransmission, that is the release of glutamate from perisynaptic astrocyte processes in an activity-dependent manner, has emerged as a potentially crucial signal-ing pathway for regulation of synaptic plasticity, yet its modes of expression and function in vivo remain unclear. We focused on two experimentally well-identified gliotransmitter patwhays: (i) modulations of synaptic release and (ii) postynaptic 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 protocol. These results have been published in Neural plasticity <a href="./bibliography.html#beagle-2016-bid38">[17]</a> and in a review targetting a biologist audience in the journal Neuroscience <a href="./bibliography.html#beagle-2016-bid39">[18]</a>.</p>
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