Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study

Figure 1

Pathways of glutamatergic gliotransmission. Perisynaptic astrocytic processes in several brain areas and different excitatory (but also inhibitory) synapses may release glutamate in a -dependent fashion. In turn, released astrocytic glutamate may increase (or decrease) synaptic neurotransmitter release by activating extrasynaptically located presynaptic receptors (magenta arrows) or contribute to postsynaptic neuronal depolarization by binding to extrasynaptic NMDA receptors (orange arrows) which mediate slow inward currents (SICs). These receptors often (but not always) contain NR2B subunits and are thus different with respect to postsynaptic NMDARs. Glutamate release by the astrocyte could be triggered either by activity from the same synapses that are regulated by the astrocyte (homosynaptic scenario) or by other synapses that are not directly reached by glutamatergic gliotransmission (heterosynaptic scenario).