Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study.
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.
Duke Scholars
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Related Subject Headings
- Synaptic Transmission
- Synapses
- Neuronal Plasticity
- Neurology & Neurosurgery
- Models, Neurological
- Hippocampus
- Glutamic Acid
- Astrocytes
- Animals
- 5202 Biological psychology
Citation
Published In
DOI
EISSN
Publication Date
Volume
Start / End Page
Location
Related Subject Headings
- Synaptic Transmission
- Synapses
- Neuronal Plasticity
- Neurology & Neurosurgery
- Models, Neurological
- Hippocampus
- Glutamic Acid
- Astrocytes
- Animals
- 5202 Biological psychology