Fig. 4. Schematic diagram depicting the astrocytic localization and function of Best1 in normal condition and pathological condition. In normal condition (left), Best1 is preferentially expressed at the microdomains of hippocampal astrocytes adjacent to glutamatergic synapses. The opening of Best1 channel by astrocytic Ca2+ increase mediates glutamate release, and which results in activation of NMDAR and NMDAR-dependent potentiation of synaptic responses. In pathological condition such as Alzheimer's disease model (right), Best1 is redistributed to soma and processes of hippocampal reactive astrocytes which have GABA. Tonically released GABA mediated by Best1 from reactive astrocytes impairs synaptic transmission, synaptic plasticity and spatial memory by inhibiting dentate granule cell excitability.
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