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Vesicular inhibitory amino acid transporter (SLC32A1, also known as VGAT or VIAAT) is an integral synaptic vesicle membrane protein responsible for transporting the inhibitory neurotransmitters GABA and glycine from the cytoplasm into synaptic vesicles of GABAergic and glycinergic neurons, as well as some endocrine cells[1][2][5][7]. This accumulation enables their regulated, exocytosis-mediated release during inhibitory neurotransmission in the central nervous system. SLC32A1 is unique in its function: it exchanges cytosolic GABA or glycine for vesicular protons, utilizing the electrochemical gradient generated by a vesicular H+-ATPase, with additional chloride co-transport required for optimal function[2][4][5]. Pathogenic variants of SLC32A1 can impair GABA/glycine filling of synaptic vesicles, leading to severe neurodevelopmental disorders and epilepsy in humans[3]. The protein is a specific molecular marker for GABAergic neurons and a member of the amino acid/polyamine transporter family II within the broader SLC (solute carrier) superfamily[5]. Currently, it is not a direct target for clinically approved drugs.
Vesicular uptake/antiport of GABA or glycine (from cytoplasm into synaptic vesicle) in exchange for protons; vesicular stoichiometry also involves chloride co-transport for GABA/glycine loading[2][4][5].
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