Abstract
The functional role of astrocyte calcium signaling in brain information processing was intensely debated in recent decades. This interest was motivated by high resolution imaging techniques showing highly developed structure of distal astrocyte processes. Another point was the evidence of bi-directional astrocytic regulation of neuronal activity. To analyze the effects of interplay of calcium signals in processes and in soma mediating correlations between local signals and the cell-level response of the astrocyte we proposed spatially extended model of the astrocyte calcium dynamics. Specifically, we investigated how spatiotemporal properties of Ca2+ dynamics in spatially extended astrocyte model can coordinate (e.g., synchronize) networks of neurons and synapses.
Highlights
The functional role of astrocyte calcium signaling remains intensely debated
We describe three effects resulting from the influence of the gliotransmitters on the synapse: (i) potentiation of presynaptic release probability due to glutamate acting on presynaptic NMDARs; (ii) depression of presynaptic release probability due to glutamate acting on presynaptic metabotropic glutamate receptors (mGluRs); and (iii) increase of the postsynaptic currents due to D-serine modulation of the postsynaptic NMDA receptors
Let us consider the dynamics of single tripartite synapse without influence of the gliotransmitters on the synaptic signals in all compartments in the 100-ms time window) (Figure 4C) and corresponding time trace of the intracellular calcium concentration in soma (Figure 4D), it happens that the calcium response in the soma occurs as the result of a space–time integration of calcium fluctuations in the processes of the astrocyte
Summary
One of the principal reasons for such a debate is that the astrocytic Ca2+ dynamics possesses high complexity which was confirmed by new experimental approaches to study the signaling of astrocytes at qualitatively new spatial-temporal resolutions (Volterra et al, 2014; Bindocci et al, 2017; Wu et al, 2018) Another reason was the evidence of bi-directional astrocytic regulation of neuronal activity referred as gliotransmission [Ca2+-dependent release of neurotransmitters (glutamate, D-serine, ATP) by astrocytes] (Araque et al, 2014; Bazargani and Attwell, 2016; Fiacco and McCarthy, 2018; Savtchouk and Volterra, 2018). Clustering of astrocytic receptors, targeted by synaptically released neurotransmitters at points of contact of synapses with astrocytic processes (Di Castro et al, 2011; Panatier et al, 2011; Arizono et al, 2012) provides spatially confined sites of IP3 production, whose differential activation could result in rich spatiotemporal IP3 and Ca2+ dynamics (Volterra et al, 2014)
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