Figure 9.

Schematic model showing complementary modalities of NMDAR–GABA_AR interactions in MNCs. Activation of sNMDARs by synaptically released glutamate (1a), or activation of eNMDARs by ambient extracellular glutamate levels (1b) controlled by astrocyte GLT1 transporters (1c), results in an increase in [Ca²⁺]_i (1d). The Δ[Ca²⁺]_i leads to activation of kinase activity (2a), resulting in turn in potentiation of postsynaptic GABA_ARs (2b). In parallel, the Δ[Ca²⁺]_i stimulates NO synthase activity (3a), resulting in NO production and retrograde diffusion in the synaptic cleft (3b), stimulating in turn presynaptic release of GABA (3c).