A computational study of astrocytic glutamate influence on post-synaptic neuronal excitability
Fig 3
Presynaptic neuron-astrocyte interaction for presynaptic 10 Hz simulation (top) for different basal [Glu]ast.
(a) The synaptic glutamate concentration resulting from presynaptic release and astrocytic uptake, indicates a longer time course of glutamate in synaptic cleft where [Glu]ast is increased due to slower uptake by EAAT2. Inset: closer view of synaptic glutamate concentration. (b) Higher activation of mGluRs in response to prolonged synaptic glutamate (Inset: closer view of astrocytic mGluRs activation) resulting in (c) perturbation of IP3 production and degradation, activating Ca2+ ER channels and resulting [Ca2+] elevations in the (d) perisynaptic process. (e) The release of glutamate by astrocyte in response to super-threshold Ca2+ elevations and enhanced by increased cytosolic [Glu]. (f) Increase in astrocytic membrane potential (Vast) as a result of synaptic-driven currents.