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Schematic representation of GABA release from astrocytes in AD pathology. (1) Amyloid plaques evoke an enhanced activation of the monoamine oxidase MAOB (2) to induce the GABA synthesis using putrescine as a substrate (3). GABA is released from astrocytes via the anion channel BEST1 (4). GABA released as a gliotransmitter acts on postsynaptic (5) or presynaptic (6) GABA receptors (GABAR) to impact synaptic transmission. Arrows indicate increases.
