Modulation of synaptic plasticity by glutamatergic gliotransmission: A modeling study

TL;DR

This modeling study explores how glutamatergic gliotransmission from astrocytes influences synaptic plasticity, revealing it can significantly alter spike-timing-dependent plasticity and shift the balance between potentiation and depression.

Contribution

The paper introduces a biophysical model demonstrating the potential of astrocyte-mediated glutamate release to modulate synaptic plasticity in novel ways.

Findings

Glutamatergic gliotransmission can affect short- and long-term plasticity.

Astrocyte glutamate release can reverse spike-timing-dependent plasticity outcomes.

Model predicts profound impact of astrocytes on synaptic regulation.

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 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.