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Gamma‐aminobutyric acid transporters are a family of membrane proteins responsible for the reuptake and regulation of the inhibitory neurotransmitter gamma‐aminobutyric acid (GABA) from the synaptic cleft. They belong to the solute carrier 6 family and function as sodium/chloride-dependent symporters. The main subtypes—GAT1, GAT2, and GAT3—are differentially expressed throughout neurons and glial cells in the brain. By controlling extracellular levels of GABA during both basal activity and synaptic transmission, these transporters play a critical role in maintaining inhibitory tone within neural circuits. Pharmacological inhibition—such as by tiagabine—is clinically exploited to treat epilepsy by enhancing synaptic inhibition through increased ambient levels of extracellular GABA. Structural studies reveal that these transporters have 12 transmembrane domains with key sites for substrate binding and inhibitor interaction.
Inhibition of GABA reuptake, increasing extracellular levels of inhibitory neurotransmitter; Modulation of synaptic inhibition by altering presynaptic and extrasynaptic GABA concentrations
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