Vesicular inhibitory amino acid transporter (VGAT) (VGAT)

The Vesicular inhibitory amino acid transporter (VGAT), also known as SLC32A1 or VIAAT, is a transmembrane protein responsible for the uptake of inhibitory neurotransmitters, specifically gamma-aminobutyric acid (GABA) and glycine, into synaptic vesicles [1, 4]. This transport process is essential for the storage and subsequent release of these neurotransmitters into the synaptic cleft, thereby mediating inhibitory signaling in the central nervous system [1, 2]. VGAT is driven by a proton electrochemical gradient maintained by the vacuolar H+-ATPase [4]. Dysregulation of VGAT function or mutations in the SLC32A1 gene have been linked to several neurological disorders, including early-onset epilepsy, neurodevelopmental delay, and potentially psychiatric conditions such as schizophrenia [2, 3]. While VGAT is a critical component of inhibitory neurotransmission, there are currently no FDA-approved drugs that selectively target it; however, it remains a significant subject of research for modulating brain excitability [3]. Experimental compounds like Evans Blue are used in laboratory settings to inhibit its activity and study its role in synaptic physiology [4]. References: [1] UniProt (Q9H598); [2] NCBI Gene (140679); [3] PubMed (28803338); [4] PubMed (9354326).

Other names

SLC32A1VIAATVesicular GABA transporterSolute carrier family 32 member 1

Inhibition of vesicular neurotransmitter uptake into synaptic vesicles, thereby reducing the amount of GABA or glycine available for release [4].