Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study

Figure 2

Biophysical modeling of a gliotransmitter-regulated synapse. ((a)–(c)) Model of synaptic release. Incoming presynaptic spikes (a) increase intrasynaptic levels which directly control the probability of release of available neurotransmitter resources ((b), Nt. Rel. Pr.) and decrease, upon release, the fraction (or probability) of neurotransmitter-containing vesicles available for release (Avail. Nt. Pr.). Each spike results in release of a quantum of neurotransmitter from the synapse ((c), Released Nt.) whose concentration in the perisynaptic space decays exponentially. Synapse parameters: s, s, and . Stimulation by Poisson-distributed APs with an average rate of 5 Hz. ((d)–(f)) Model for astrocyte activation. Synaptically released neurotransmitter in the perisynaptic space (d) binds astrocytic receptors ((e), Bound Ast. Rec.), resulting in production which triggers signaling in the astrocyte (f). This latter also depends on the fraction of deinactivated receptors/ channels (Deinact. Rs) on the astrocyte ER membrane (see Appendix A.1). ((g)–(i)) Model for gliotransmitter release. The increase of astrocytic beyond a threshold concentration ((g), cyan dashed line) results in the release of a quantum of gliotransmitter, which decreases the probability of further release of gliotransmitter ((h), Avail. Gt. Pr.) while transiently increasing extracellular gliotransmitter concentration ((i), Released Gt.). Model parameters as in Table 1.