GABAtransporterien

GABAtransporterien, often abbreviated as GATs, are a family of transmembrane proteins responsible for the reuptake of gamma-aminobutyric acid (GABA) from the extracellular space into neurons and glial cells. GABA is the primary inhibitory neurotransmitter in the mammalian central nervous system, and its precise regulation is crucial for maintaining neuronal excitability and preventing seizures. GATs play a vital role in terminating GABAergic neurotransmission by removing GABA from the synaptic cleft, thus controlling the duration and extent of inhibition.

There are four known subtypes of GABAtransporterien in mammals: GAT1, GAT2, GAT3, and BGT-1. GAT1 is the most widely studied and is primarily located on presynaptic GABAergic nerve terminals, where it efficiently clears GABA from the synaptic cleft. GAT2 is predominantly found in glial cells and some neurons, particularly in the brainstem and spinal cord. GAT3 is also expressed in glial cells and some neurons, with a distribution pattern that complements GAT1. BGT-1 is a high-affinity transporter for the structurally related molecule $\beta$-alanine, but it also transports GABA, especially in glial cells.

The activity of GABAtransporterien is essential for normal brain function. Dysregulation of GATs has been implicated in various neurological and psychiatric disorders, including epilepsy, anxiety disorders, and depression. For instance, inhibition of GAT1 activity can enhance GABAergic neurotransmission and has been explored as a therapeutic strategy for epilepsy. Conversely, impaired GAT function might contribute to conditions characterized by reduced inhibition. The specific localization and substrate affinities of the different GAT subtypes contribute to the complex spatiotemporal regulation of GABAergic signaling throughout the brain.