[5][6][7] It mediates gamma-aminobutyric acid's translocation from the extracellular to intracellular spaces within brain tissue and the central nervous system as a whole.

[20] A study on genetic absence epilepsy rats from Strasbourg (GAERS) found that poor GABA uptake by GAT1 caused an increase in tonic current of GABAA.

In the two most understood forms of absence epilepsy, synaptic GABAA receptors including GAT1 play a major role in seizure development.

Blocking GAT1 in non-epileptic control (NEC) rats caused tonic current to increase to a rate similar to that of GAERS of the same age.

[23][24][25] This article incorporates text from the United States National Library of Medicine, which is in the public domain.